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1
Pathare, 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.
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Thesis (Ph.D.)--University of Florida, 2005.Typescript. Title from title page of source document. Document formatted into pages; contains 171 pages. Includes Vita. Includes bibliographical references.
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Baker, 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.
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Thesis (Ph. D.)--West Virginia University, 2007.Title from document title page. Document formatted into pages; contains xii, 270 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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Xia, Jinjun. "Optical characterization of skeletal muscles." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/5965.
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Thesis (Ph. D.)--University of Missouri-Columbia, 2007.The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on October 18, 2007) Vita. Includes bibliographical references.
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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/.
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Thesis (M.S.)--California Polytechnic State University, 2008."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.
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Lewis, Trevor M. "Anion pathway in the sarcoplasmic reticulum of skeletal muscle /." Adelaide, S. Aust, 1993. http://web4.library.adelaide.edu.au/theses/09PH/09phl676.pdf.
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Watt, Kevin. "Regualtion of myogenesis and skeletal muscle size by the myostatin-Smad and mammalian Hippo signalling transduction pathways." Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=62160.
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Arc-Chagnaud, Coralie. "Regulation of antioxidant defenses in the prevention of skeletal muscle deconditioning." Thesis, Montpellier, 2019. http://www.theses.fr/2019MONT4005.
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Le système musculaire joue un rôle primordial dans l’homéostasie de l’organisme. Il est impliqué dans différentes fonctions indispensables aux activités de la vie quotidienne telles que la production de mouvement, la locomotion, le maintien postural et l’équilibre. La qualité du tissu musculaire est donc primordiale dans le maintien de la qualité de vie et, à long terme, à la longévité. L'hypoactivité et le vieillissement sont deux situations qui entraînent le déconditionnement musculaire, et qui partagent une caractéristique commune: une perte de force musculaire, une atrophie et la modification du typage musculaire, ainsi que l'accumulation de tissu adipeux intramusculaire. Aujourd'hui, il existe de nombreuses données dans la littérature indiquant un lien entre le stress oxydant et le déconditionnement musculaire. Le but de cette thèse était d'évaluer l'impact de la modulation des défenses antioxydantes sur la prévention du déconditionnement musculaire. Cela a été étudié sous deux angles, l'un dans le contexte du vieillissement, et le second dans un contexte d'hypoactivité. La première étude avait pour but d'évaluer la fragilité chez un modèle souris âgées, utilisant un groupe de souris WT et un groupe de souris transgéniques sur-exprimant l'enzyme G6PD. Nous avons évalué des paramètres de qualité musculaire et de stress oxydant et avons réalisé une analyse transcriptomique à partir d'échantillons musculaires des souris de chacun des deux groupes. La seconde étude a été conduite dans le but d'évaluer les effets d'un cocktail enrichi en composés anti-oxydants et anti-inflammatoires, durant deux mois d'hypoactivité (modèle Bedrest). Nos résultats ont démontré l’inefficacité de cette supplémentation sur la prévention de la perte de masse et de force musculaire. De plus, les données concernant les mécanismes moléculaires ont démontré une altération des processus de récupération chez les sujets supplémentés.Les conclusions de nos études donnent des pistes sur les stratégies anti-oxydantes les plus appropriées contre le déconditionnement musculaire. Il semble préférable de intéresser à la stimulation des systèmes de défenses endogènes, plutôt que de se centrer sur une supplémentation nutritionnelle exogène. Néanmoins, la complexité des voies de signalisation redox requièrent une meilleure compréhension pour optimiser les mesures de prévention afin de limiter la perte de fonction musculaireMusculoskeletal 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
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Boss, Matthew John. "Analysis-ready isogeometric model of skeletal muscles." Thesis, University of Iowa, 2012. https://ir.uiowa.edu/etd/2827.
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New methods are employed to develop an anatomically accurate, analysis-ready isogeometric model of skeletal muscles. Current modeling techniques for the analysis of skeletal muscles include the utilization of finite element meshing, which inherently poses a few well-known problems that provide motivation for isogeometric analysis. In addition to those issues, standard FEA meshing cannot preserve smooth geometries, therefore the accuracy of the foregoing model and analysis is reduced. Moreover, there is no easy means to characterize fiber direction in the FEA framework due to discontinuities at element boundaries. Additionally, material property distributions such as the transition of the muscle-tendon complex along the longitudinal axis through FEA are prescribed on an element by element basis, leading to abrupt, unrealistic property changes at element boundaries. The current research builds on the idea of an isogeometric tensor-product rod using harmonic coordinates and NURBS [1]. Through a direct comparison between a meshed, FEA model and the tensor-product rod model, it can be shown that the tensor-product rod model preserves smoothness, enhancing the geometric representation passed through to analysis while reducing the total DOF of the model. Muscle fibers can be easily implemented as parametric lines with muscle-specific orientations along the muscles' longitudinal axis that match distinct fiber orientations existent within common skeletal muscles. This technique not only allows for the representation of perfectly parallel-fibered structures, but also those that do not directly follow the longitudinal axis such as a helical twist. Utilizing this geometric method also provides the framework for implementing material properties using an interpolative-style scheme. Varying properties at specific longitudinal control point cross-sections near muscle termination areas can be designated to more accurately represent the muscle-tendon complex. These new techniques allow for the creation of an analysis-ready, realistic skeletal muscle model of the male human arm. The model contains 28 muscles complete with muscle-specific geometric, fiber, and heterogeneous property characterizations all compiled into a complete "digital muscle library."
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Yeung, Wai Ella, and 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.
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Mazelet, Lise. "The role of contraction in skeletal muscle development." Thesis, Queen Mary, University of London, 2015. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8960.
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The aim of this project was to determine the role of contraction in skeletal muscle development. The role of the initial spontaneous contractions observed in zebrafish embryos from 17 to 24 hours post fertilisation was examined. Genetic and pharmacologic approaches were used to study paralysis-induced disruption of skeletal muscle structure and function and subsequently determine the role of contraction. The structural and functional characteristics of developing skeletal muscles were found to be regulated by a dual mechanism of both movement-dependent and independent processes, in vivo. Novel data demonstrates that contraction controls sarcomere remodelling, namely regulation of actin length, via movement driven localisation of the actin capping protein, Tropmodulin1. Myofibril length was also shown to be linked to the mechanical passive property, stretch, with lengthening leading to an increase of the muscle’s ability to stretch. In addition, myofibril bundling and the myofilament lattice spacing, responsible for active tension generation via cross-bridge formation, were shown to be unaffected by paralysis and thus, movement-independent processes. Furthermore, the mechanism of the contraction-driven myofibril organisation pathway at the focal adhesion complexes (FAC), was shown to be different in zebrafish compared to mammals, with mechanosensing revolving around the Src protein rather than Fak. In summary, the role of contraction was established as a critical driver of myofibril organisation and passive tension in the developing zebrafish skeletal muscle. Passive tension regulates muscle function by determining its operational range ensuring that the needs of locomotion are met. Furthermore, investigation of FAC’s role in the contractiondriven myofibril organisation pathway led to the discovery of a novel function for Src in zebrafish somitogenesis. These two findings (i) that contraction is a driver of myofibril organisation and (ii) that Src is a key protein of the skeletal muscle development provides the potential for new therapeutic approaches in humans.
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Watt, Kevin. "Regulation of myogenesis and skeletal muscle size by the myostatin-Smad and mammalian Hippo signalling transduction pathways." Thesis, University of Aberdeen, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=62160.
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The aims of this thesis were to 1) investigate the effect of SB431542 in vitro and ex vivo as a novel approach towards promoting the functional hypertrophy of skeletal muscle by inhibiting the myostatin-Smad pathway, 2) to investigate the expression and function of the Yes-associated protein (Yap) in skeletal muscle and C2C12 cells as a novel regulator of C2C12 differentiation and 3) to generate a GFP-RCASBP-hYAP1 S127A retrovirus to allow the study of the function of Yap in skeletal muscle differentiation in vivo. The results presented in this thesis show that SB431542 promotes the hypertrophy of C2C12 myotubes and mature Xenopus skeletal muscle fibres. However, SB431542 treatment also results in a reduction in specific force of mature Xenopus muscle fibres suggesting that SB431542 is not suitable as a treatment for skeletal muscle atrophy. These results also show that Yap is expressed in mouse skeletal muscle in vivo and that Yap is a novel regulator of C2C12 differentiation. Finally, these results descried the generation of a GFP-RCASBP-hYAP1 S127A retrovirus that can be used to assess the role of Yap in vivo during skeletal muscle formation in the chick embryo. Together, these results suggest that Yap is a novel regulator of C2C12 differentiation that should be studied as a potential therapeutic target in musculoskeletal diseases.
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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.
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Thesis (Ph.D.)--University of Wollongong, 2004.Typescript. 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.
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Smith, Cheryl A. "Skeletal muscle injury, fibrosis and transforming growth factor-[beta]." Morgantown, W. Va. : [West Virginia University Libraries], 2000. http://etd.wvu.edu/templates/showETD.cfm?recnum=1744.
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Thesis (Ph. D.)--West Virginia University, 2000.Title from document title page. Document formatted into pages; contains xii, 146 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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Yao, Yan-Dong. "Acoustic myography : the signal from contracting skeletal muscles." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321718.
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Ranasinghesagara, Janaka C. Yao Gang. "Optical reflectance in fibrous tissues and skeletal muscles." Diss., Columbia, Mo. : University of Missouri--Columbia, 2008. http://hdl.handle.net/10355/6629.
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Title from PDF of title page (University of Missouri--Columbia, viewed on March 8, 2010). The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file. Dissertation advisor: Dr. Gang Yao. Vita. Includes bibliographical references.
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Archer, Akibi A. A. "Two dimensional spatial coherence of skeletal muscle's natural vibrations during voluntary contractions." Thesis, Georgia Institute of Technology, 2010. http://hdl.handle.net/1853/42803.
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Low frequency mechanical vibrations (<100 Hz) are naturally generated by skeletal muscles during voluntary contractions. Recording of these vibrations at the muscle surface are called surface mechanomyograms (S-MMGs). In this study, S-MMGs were recorded over a 3 x 5 grid of skin mounted accelerometers on the biceps brachii muscle during submaximal voluntary isometric contractions with the arm in a pronated position for ten healthy and young male subjects with no overt sign of neuromuscular diseases. For a given pair of accelerometers, the spatial coherence of S-MMG is a measure of the similarity of the S-MMG signals propagating between those two sensors. Two common techniques to estimate the spatial coherence for narrowband S-MMG signals, namely the magnitude squared coherence function and the maximum of the time-domain cross-correlation function, were found to yield similar results. In particular, high spatial coherence values were measured for sensor pairs aligned along the proximal to distal ends of the biceps, i.e. the longitudinal direction. On the other hand, the spatial coherence values for sensor pairs oriented perpendicular to the muscle fiber, i.e. along the transverse direction, were found to be significantly lower. This finding indicates that coherent S-MMGs were mainly propagating along the muscle fibers direction (longitudinal) of the biceps brachii within a frequency band varying between 10Hz to 50Hz. Additionally, the spatial coherence of S-MMGs along the longitudinal direction was found to decrease with increasing frequency and increasing sensor separation distance and to increase with contraction level varying between 20% to 60% of the maximum contraction level.
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Tomc, Lyn Kathryn. "Role of MEF2 proteins in the activation of the c-jun and MCK genes in skeletal muscle /." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/MQ56210.pdf.
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Ravenscroft, Gianina. "A therapeutic approach for the skeletal muscle a-actin based congenital myopathies." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2009. http://theses.library.uwa.edu.au/adt-WU2010.0049.
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[Truncated abstract] Mutations in the skeletal muscle -actin gene (ACTA1) have been shown to be one cause of a broad group of muscle disorders all termed the congenital myopathies. Over 170 different mutations have now been identified across all 6 coding exons of ACTA1 in patients presenting with muscle weakness and any one or more of the following histopathological features: nemaline rods, intranuclear rods, fibre-type disproportion, excess of thin filaments and central cores. While the identification of the causative gene has been of great comfort for affected patients and their families, with pre-natal genetic testing becoming available, the ultimate aim is to develop a therapy for these disorders. Of the therapies currently being explored for the muscular dystrophies, up-regulation of an alternative gene seemed to be one of the most promising avenues for treatment of the ACTA1 diseases. Up-regulation of utrophin, the foetal homologue of dystrophin, has been shown to be a promising therapy for the treatment of Duchenne muscular dystrophy. The main aim of my research was to determine whether up-regulation of cardiac -actin, the predominant -actin expressed in foetal skeletal muscle and in the adult heart, could be used as a therapy for the ACTA1 diseases. A proof-of-concept experiment was performed whereby skeletal muscle -actin knock-out (KO) mice (all of which die by postnatal day 9) were crossed with transgenic mice over-expressing cardiac -actin (known as Coco mice) in postnatal skeletal muscle. ... While patients that are ACTA1 nulls have been identified in a number of mainly consanguineous populations, the majority of ACTA1 mutations result in dominant disease in which the mutant protein interferes with the function of the wild-type skeletal muscle -actin. Research described in this thesis also focuses on characterizing two transgenic mouse models of dominant ACTA1 disease at the ultra-structural, cellular and functional level; this is the first step towards a proof-of-concept experiment to determine whether cardiac -actin up-regulation can dilute out the pathogenesis of dominant ACTA1 disease. It has long been noted that patients with ACTA1 disease do not have ophthalmoplegia, even in the most-severely affected individuals. Protein analysis performed on extraocular muscle (EOM) biopsies obtained from humans, sheep and pigs showed that the EOMs co-express cardiac and skeletal muscle -actin, with cardiac -actin comprising 70 % of the striated -actin pool. Thus we propose that sparing of the EOMs in ACTA1 disease is at least in part due to cardiac -actin diluting out the pathogenesis associated with expression of the mutant skeletal muscle -actin. This finding provides further support for the hypothesis that dilution of mutant skeletal muscle -actin in dominant ACTA1 disease by up-regulation of cardiac -actin may be a viable therapy for this group of devastating muscle diseases. The research contained herein has advanced the understanding of the pathobiology of skeletal muscle -actin diseases and provides strong evidence in support of cardiac -actin up-regulation as a promising therapy for these diseases.
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Panenic, Robert. "TTX-induced disuse of mammalian skeletal muscle." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=59523.
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Previous reports of the effects of tetrodotoxin (TTX)-induced muscular disuse have demonstrated alterations in muscle force, speed, and fatiguability that might suggest changes in the quality of contractile proteins. These studies were extended to the effects of TTX-induced disuse on the Ca$ sp{2+}$-activation characteristics of myofibrillar ATPase of the rat gastrocnemius. Atrophic responses after TTX treatment were as previously reported with a significant decrease in left gastrocnemius weight (g) compared to the control-pump (C) group (1.25 $ pm$ 0.04 for C vs 0.72 $ pm$ 0.04 for TTX, X $ pm$ SEM, p $ leq$ 0.01). Myofibrillar protein yield (mg$ cdot$g$ sp{-1}$ wet weight) was also depressed (92.8 $ pm$ 4.6 for C vs 70.3 $ pm$ 3.7 for TTX; p $ leq$ 0.01). Maximum ATPase of myofibrils (nmol Pi$ cdot$mg$ sp{-1} cdot$min$ sp{-1}$) was decreased (424 $ pm$ 46 for C vs 199 $ pm$ 27 for TTX, p $ leq$ 0.01). Furthermore, the Hill n which reflects the cooperative aspects of Ca$ sp{2+}$-activation of the myofibrillar ATPase was significantly depressed (1.58 $ pm$ 0.07 for C vs 1.29 $ pm$ 0.09 for TTX; p $ leq$ 0.05) after TTX treatment. The results of the present study suggest that muscle perturbations that result from TTX-induced disuse are at least partially related to changes in the myofibrillar fraction.
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Bishop, Derron L. "Alterations in Z-line thickness following fast motoneuron transplantation onto slow twitch skeletal muscle fibers." Virtual Press, 1995. http://liblink.bsu.edu/uhtbin/catkey/935926.
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Differentiation of skeletal muscle fibers into fast and slow twitch appears to be under control of the stimulation pattern imparted by motoneurons innervating these muscle fibers. Fast twitch muscle fibers receive intense stimulation for brief periods of time while slow twitch muscle fibers receive less intense stimulation for much longer periods of time. This study examined thickness of Zlines in dually innervated skeletal muscle fibers of slow twitch soleus muscle following transplantation of the fast extensor digitorum longus (EDL) nerve onto the surface of the soleus. Eight individual dually innervated fibers were dissected from four transplanted mouse soleus muscles and examined with a transmission electron microscope. Z-lines in these dually innervated fibers were thinner (mean = 83 nm) than control soleus (mean = 123 nm) and thicker than control EDL (mean = 57 nm). A significant difference (p< .002) was also found between Z-line thickness near the foreign EDL endplate (mean = 81 nm) versus the original soleus endplate (mean = 85 nm). These results suggest the factors controlling protein synthesis in skeletal muscle fibers have both a global and localized effect.Department of Physiology and Health Science
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Watkins, Thomas C. "Characterization of Skeletal Muscle Antibodies in Patients with Autoimmune Rippling Muscles and Myasthenia Gravis." Youngstown State University / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ysu997728299.
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Ning, Jie. "Estrogen receptor [alpha] and [beta] knock-out effects on skeletal muscle in mature female and male mice, and aromatase knock-out effects on skeletal muscle in mature male mice." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/6273.
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Thesis (M.S.)--University of Missouri-Columbia, 2007."August 2007" The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. Includes bibliographical references.
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Rossi, Alberto. "Novel/ancient myosins in mammalian skeletal muscles: MYH7B and MYH15." Doctoral thesis, Università degli studi di Padova, 2010. http://hdl.handle.net/11577/3427353.
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Myosin, the molecular motor responsible for muscle contraction, exists in multiple forms which dictate muscle properties, such as shortening velocity and contractile force. Until ten years ago only eight sarcomeric myosin heavy chain (MYH) genes, associated into two highly conserved gene clusters, were known to be present in mammals (Weiss et al., 1999a; Weiss et al., 1999b). Two tandemly arrayed genes, located in human chromosome 14, code for the cardiac myosins, α- and β-MYH, the latter being also expressed in slow skeletal muscle. Another gene cluster, located in human chromosome 17, codes for the six skeletal myosins, including the adult fast 2A-, 2X- and 2B-MYH, the developmental embryonic and neonatal/perinatal isoforms, and MYH13, an isoform expressed specifically in extraocular (EO) muscles. The completion of the Human Genome Project almost ten years ago showed that the mammalian genome contains three additional genes coding for sarcomeric MYHs. One of these, MYH16, was shown to code for a myosin expressed in jaw muscles of carnivores and primates but is a pseudogene in humans (Stedman et al., 2004). However nothing is known concerning the two other novel MYHs: MYH7B and MYH15. Therefore, we asked whether these two genes are expressed in mammalian striated muscles. We found that MYH7B and MYH15 orthologs are present in frogs and birds, coding for chicken slow myosin 2 and ventricular MYH, respectively, whereas only MYH7B orthologs have been detected in fish. In all species the MYH7B gene contains a microRNA, miR-499. We report that in rat and mouse, MYH7B and miR-499 transcripts are detected in heart, slow muscles and extraocular (EO) muscles, whereas MYH7B protein is detected only in a minor fiber population in EO muscles, corresponding to slow-tonic fibers, and in bag fibers of muscle spindles. MYH15 transcripts are detected exclusively in EO muscles and the MYH15 protein is present in most fibers of the orbital layer of EO muscles and in the extracapsular region of nuclear bag fibers. During development, MYH7B is expressed at low levels in skeletal muscles, heart and all EO muscle fibers but disappears from most fibers, except the slow-tonic fibers, after birth. In contrast, MYH15 is absent in embryonic and fetal muscles and is first detected after birth in the orbital layer of EO muscles.
We trace the evolutionary history of these myosins in vertebrates and show that MYH15 undergoes drastic changes in structure and function in mammals compared to lower vertebrates, whereby the same gene codes for a myosin used to pump blood in frogs and birds or to control eye movements in mammals, thus providing a striking case of evolutionary tinkering (Jacob, 1977). We show that the other gene, MYH7B, contains a specific microRNA, miR-499, which is conserved in all vertebrate classes, and we suggest that this may account for the striking mismatch, unprecedented in sarcomeric myosins, between the expression of transcript, high in slow and cardiac muscles, and corresponding protein, restricted to slow-tonic fibers in EO muscles. Finally, we show that these novel myosins undergo striking changes during early postnatal development, namely during the critical period when visual experience is required for the correct maturation of both sensory visual and oculomotor systems. In addition, we find that these myosins are also expressed in intrafusal fibers of muscle spindles, the proprioceptive sensory organs embedded in most skeletal muscles.
In conclusion, the characterization of the expression pattern of MYH7B and MYH15 provides a definitive picture of MYH expression in mammalian striated muscle, thus completing the inventory of MYH isoforms involved in sarcomeric architecture of skeletal muscles. We also establish the existence of slow-tonic MYH as a specific gene product, providing an unambiguous molecular basis to study the contractile properties of slow-tonic fibers in mammals.La miosina è il motore molecolare responsabile della contrazione muscolare ed esiste in diverse forme che riflettono alcune proprietà del muscolo, come ad esempio la velocità di accorciamento e la forza di contrazione. Fino a dieci anni fa solo otto catene pesanti della miosina sarcomerica (MYH) erano note essere presenti nel muscolo scheletrico dei mammiferi, suddivise in due gruppi altamente conservati (Weiss et al., 1999a; Weiss et al., 1999b). Un gruppo si trova nel cromosoma umano 14 e codifica per le due miosine cardiache alpha e beta, l’ultima delle quali è espressa oltre che nel cuore anche nei muscoli lenti. Un altro gruppo si trova nel cromosoma umano 17 e codifica per le sei miosine scheletriche, che includono le isoforme veloci 2A-, 2X, 2B-MYH, la embrionale e la neonatale espresse nei muscoli nelle fasi dello sviluppo, e la MYH13, un'isoforma espressa esclusivamente nei muscoli extraoculari (EO). Il completamento del Progetto Genoma Umano, circa dieci anni fa, ha rivelato che oltre a questi due gruppi di miosine cardiache e scheletriche, il genoma umano contiene altri tre geni della catena pesante della miosina sarcomerica: MYH7B (chiamata anche MYH14), MYH15 e MYH16. La MYH16 è espressa nei muscoli masticatori dei carnivori e primati, ma è uno pseudogene negli umani (Stedman et al., 2004). Tuttavia, nulla è noto circa l’espressione degli altri due geni: MYH7B e MYH15. Pertanto, ci siamo posti la domanda se questi due geni fossero espressi nei muscoli striati dei mammiferi. Abbiamo constatato che ortologhi di MYH7B e MYH15 sono presenti nelle rane e negli uccelli, e, rispettivamente, codificano per la miosina lenta di tipo 2 e la miosina ventricolare, mentre solo ortologhi della MYH7B sono presenti nei pesci. In tutte le specie il gene MYH7B contiene al suo interno un microRNA, il miR-499. In questo studio abbiamo dimostriamo che in topo e ratto i trascritti di MYH7B e miR-499 sono espressi nel cuore, nei muscoli lenti e EO, mentre la proteina MYH7B è presente esclusivamente in una sottopopolazione di fibre dei muscoli EO corrispondenti alle fibre slow-tonic e nelle fibre nuclear bag dei fusi neuromuscolari. Il trascritto di MYH15 è espresso esclusivamente nei muscoli EO e la proteina MYH15 è presente nella maggioranza delle fibre nello strato orbitale dei muscoli EO e nella regione extracapsulare delle fibre bag dei fusi neuromuscolari. Durante lo sviluppo, la MYH7B è presente come trascritto a bassi livelli nei muscoli scheletrici, cuore e muscoli EO, tuttavia dopo la nascita scompare limitando la sua espressione proteica solo nelle fibre slow-tonic. Al contrario, la MYH15 è assente durante lo sviluppo fetale ed embrionale, ed è presente solo dopo la nascita nello strato orbitale dei muscoli EO. Abbiamo analizzato la storia evoluzionistica di queste miosine nei vertebrati e abbiamo dimostrato che la MYH15 subisce drastici cambiamenti nella struttura e funzione nei mammiferi rispetto ai vertebrati inferiori; infatti, lo stesso gene che codifica per una miosina espressa nel cuore ed usata nella contrazione cardiaca nelle rane, codifica per una miosina espressa nei muscoli EO ed utilizzata per il controllo del movimento degli occhi nei mammiferi; questo fenomeno rappresenta un affascinante caso di tinkerig evoluzionistico (Jacob, 1977). Abbiamo dimostrato che l’altro gene, MYH7B, contiene un microRNA, il miR-499, che è conservato in tutte le classi di vertebrati. Abbiamo ipotizzato che questo microRNA possa essere coinvolto nella differenza di espressione tra il trascritto della MYH7B, abbondante nei muscoli lenti e cardiaco, e la rispettiva proteina, limitata in una sottopopolazione di fibre nei muscoli EO. Questa differenza tra il livello di espressione di trascritto e proteina rappresenta un caso unico nella famiglia delle miosine sarcomeriche. Infine, abbiamo dimostrato che queste due miosine subiscono importanti cambiamenti nei livelli di espressione nelle due settimane successive alla nascita, un periodo durante il quale l’esperienza visiva è necessaria per il corretto sviluppo del sistema sensoriale visivo ed oculomotorio. Inoltre, abbiamo dimostrato che queste miosine sono espresse anche nelle fibre intrafusali dei fusi neuromuscolari che costituiscono il sistema sensoriale propriocettivo dei muscoli scheletrici. In conclusione, la caratterizzazione delle miosine MYH7B e MYH15 completa il quadro dell’espressione delle miosine sarcomeriche nei muscoli striati di mammifero, ridefinendo l’inventario di miosine coinvolte nell’architettura del sarcomero. Inoltre, abbiamo confermiamo definitivamente l’esistenza della miosina slow-tonic come prodotto di un gene distinto, fornendo le basi molecolari per lo studio della fisiologia di queste fibre nei mammiferi.
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Munoz, Nicole. "Glucosamine reduces glycogen storage in L6 skeletal muscle cells." Online access for everyone, 2007. http://www.dissertations.wsu.edu/Thesis/Fall2007/n_munoz_112507.pdf.
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Al-Tarrah, Mustafa. "The effect of citrate synthase on skeletal muscle metabolism." Thesis, University of Aberdeen, 2017. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=235778.
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Citrate synthase (CS) is a key mitochondrial enzyme in the tricarboxylic acid cycle (TCA). TCA provides NADH and FADH for the ETC to generate ATP through oxidative phosphorylation in muscle cells. The aim of this PhD project is to investigate the role of CS in skeletal muscle metabolism. The aim of the first study was to investigate the effects of a high fat diet (HFD, 45 % kcal fat) for 12 weeks on CS activity in the heart and gastrocnemius muscle of C57BL/6J (B6) mice and congenic (B6.A) characterised by 39% reduced CS activity. Spectrophotometric analysis of CS activity in the heart and gastrocnemius muscle revealed that HFD led to an increase in CS activity in gastrocnemius muscle but a decrease in the heart in both strains of mice. The aim of the second study was to investigate the effects of low CS activity on substrate metabolism in primary muscle cells established from B6 and B6.A mice. Primary muscle cells from both strains were incubated in radiolabelled glucose or palmitate to assess their oxidation in the mitochondria. The reduction of CS activity in B6.A muscle cells did not affect glucose and palmitate oxidation. The aim of the third study was to investigate the effects of D- and L-serine on CS activity in B6 muscle homogenates, primary muscle cells and purified CS from porcine heart. The muscle samples were incubated in D - or L-serine at 0.1 mM or 5 mM concentration and CS activity levels were assessed by spectrophotometer. D- or L-serine did not have any effect on CS activity in muscle samples. The aim of the fourth study was to investigate the effects of low CS activity on substrate metabolism in C2C12 muscle cells. Lentiviral transduction of C2C12 muscle cells with shRNA resulted in a reduction of CS activity and the metabolic pathways were assessed using XF24 Analyser, western blotting, Immunofluorescence and qRTPCR. Low CS activity was associated with a reduction in substrate oxidation by the mitochondria, an increase in glycolysis and ceramide accumulation in C2C12 muscle cells. The results highlight the significance of CS activity as a modulator of muscle metabolism.
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Whitehead, Nicholas P. (Nicholas Paul) 1975. "Factors affecting the passive mechanical properties of skeletal muscle : thixotropy and eccentric contractions." Monash University, Dept. of Physiology, 2002. http://arrow.monash.edu.au/hdl/1959.1/7883.
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Vlahovich, 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.
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Cells contain an elaborate cytoskeleton which plays a major role in a variety of cellular functions including: maintenance of cell shape and dimension, providing mechanical strength, cell motility, cytokinesis during mitosis and meiosis and intracellular transport. The cell cytoskeleton is made up of three types of protein filaments: the microtubules, the intermediate filaments and the actin cytoskeleton. These components interact with each other to allow the cell to function correctly. When functioning incorrectly, disruptions to many cellular pathway have been observed with mutations in various cytoskeletal proteins causing an assortment of human disease phenotypes. Characterization of these filament systems in different cell types is essential to the understanding of basic cellular processes and disease causation. The studies in this thesis are concerned with examining specific cytoskeletal tropomyosin-defined actin filament systems in skeletal muscle. The diversity of the actin filament system relies, in part, on the family of actin binding proteins, the tropomyosins (Tms). There are in excess of forty Tm isoforms found in mammals which are derived from four genes: α, β, γ and δTm. The role of the musclespecific Tms in striated muscle is well understood, with sarcomeric Tm isoforms functioning as part of the thin filament where it regulates actin-myosin interactions and hence muscle contraction. However, relatively little known about the roles of the many
cytoskeletal Tm isoforms. Cytoskeletal Tms have been shown to compartmentalise to form functionally distinct filaments in a range of cell types including neurons (Bryce et al., 2003), fibroblasts (Percival et al., 2000) and epithelial cells (Dalby-Payne et al., 2003). Recently it has been shown that cytoskeletal Tm, Tm5NM1 defines a cytoskeletal structure in skeletal muscle called the Z-line associated cytoskeleton (Z-LAC) (Kee et al., 2004).The disruption of this structure by over-expression of an exogenous Tm in transgenic mice results in a muscular dystrophy phenotype, indicating that the Z-LAC plays an important role in maintenance of muscle structure (Kee et al., 2004). In this study, specific cytoskeletal Tms are further investigated in the context of skeletal muscle. Here, we examine the expression, localisation and potential function of cytoskeletal Tm isoforms, focussing on Tm4 (derived from the δ- gene) and Tm5NM1 (derived from the γ-gene). By western blotting and immuno-staining mouse skeletal muscle, we show that cytoskeletal Tms are expressed in a range of muscles and define separate populations of filaments. These filaments are found in association with a number of muscle structures including the myotendinous junction, neuromuscular junction, the sarcolemma, the t-tubules and the sarcoplasmic reticulum. Of particular interest, Tm4 and Tm5NM1 define cytoskeletal elements in association with the
saroplasmic reticulum and T-tubules, respectively, with a separation of less than 90 nm between distinct filamentous populations. The segregation of Tm isoforms indicates a role for Tms in the specification of actin filament function at these cellular regions. Examination of muscle during development, regeneration and disease revealed that Tm4 defines a novel cytoskeletal filament system that is orientated perpendicular to the sarcomeric apparatus. Tm4 is up-regulated in both muscular dystrophy and nemaline myopathy and also during induced regeneration and focal repair in mouse muscle. Transition of the Tm4-defined filaments from a predominsnatly longitudinal to a predominantly Z-LAC orientation is observed during the course of muscle regeneration. This study shows that Tm4 is a marker of regeneration and repair, in response to disease, injury and stress in skeletal muscle.
Analysis of Tm5NM1 over-expressing (Tm5/52) and null (9d89) mice revealed that compensation between Tm genes does not occur in skeletal muscle. We found that the levels of cytoskeletal Tms derived from the δ-gene are not altered to compensate for the loss or gain of Tm5NM1 and that the localisation of Tm4 is unchanged in skeletal muscle of these mice. Also, excess Tm5NM1 is sorted correctly, localising to the ZLAC. This data correlates with evidence from previous investigations which indicates that Tm isoforms are not redundant and are functionally distinct (Gunning et al., 2005). Transgenic and null mice have also allowed the further elucidation of cytoskeletal Tm function in skeletal muscle. Analyses of these mice suggest a role for Tm5NM1 in glucose regulation in both skeletal muscle and adipose tissue. Tm5NM1 is found to colocalise with members of the glucose transport p fibres and analysis of both transgenic and null mice has shown an alteration to glucose uptake in adipose tissue. Taken together these data indicate that Tm5NM1 may play a role in the translocation of the glucose transport molecule GLUT4. In addition to this Tm5NM1 may play a role in adipose tissue regulation, since over-expressing mice found to have increased white adipose tissue and an up-regulation of a transcriptional regulator of fat-cell formation,
PPAR-γ.
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Judson, Robert Neil. "The role of Yes-associated protein (YAP) in skeletal muscle satellite cells and myofibres." Thesis, University of Aberdeen, 2012. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=189444.
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In spite of its post mitotic nature, skeletal muscle maintains remarkable plasticity. Muscle fibres (myofibres) are capable of large alterations in their size as well as an enormous ability to regenerate following injury – thanks to a potent population of resident stem cells (satellite cells). Deciphering the molecular signalling networks responsible for skeletal muscle growth and regeneration is of key scientific interest – not least because of the therapeutic potential these pathways may hold for the treatment of diseases such as muscular dystrophy. In this thesis, the transcriptional co-factor Yes-Associated protein (Yap), the downstream effector of the Hippo Pathway, was investigated in skeletal muscle. Using gain and loss of function approaches within in vitro, ex vivo and in vivo models, the contribution of Yap in regulating both satellite cell behaviour and myofibre growth was investigated. Yap expression and activity are dynamically regulated during satellite cell activation, proliferation and differentiation ex vivo. Overexpression of Yap increased satellite cell proliferation and maintained cells in a ‘naive’, ‘activated’ state by inhibiting myogenic commitment. Knock-down of Yap impaired satellite cell expansion, but did not influence myogenic differentiation. Yap interacts with Tead transcription factors in myoblasts to upregulate genes such as CyclinD1 and Myf5. Forced expression of Yap eventually led to the oncogenic transformation of myoblasts in vitro. Contrary to predictions, constitutive expression of Yap under an inducible muscle-specific promoter in adult mice failed to induce growth and instead led to muscle wasting, atrophy and degeneration – providing evidence against the notion that Yap represents a universal regulator of tissue growth. These data provide the first insight into the function of Yap in skeletal muscle. Results highlight a novel role for Yap in regulating myogenic progression in satellite cells, as well as its propensity to induce oncogenic transformation. The precise function of Yap in adult myofibres remains unclear however, data presented here demonstrates clear cell-type specific roles for Yap compared to observations made in other tissues.
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Kjellgren, Daniel. "Human extraocular muscles : molecular diversity of a unique muscle allotype." Doctoral thesis, Umeå : Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-260.
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Yu, Ji-Guo, Jing-Xia Liu, Lena Carlsson, Lars-Eric Thornell, and Per S. Stål. "Re-evaluation of sarcolemma injury and muscle swelling in human skeletal muscles after eccentric exercise." Umeå universitet, Idrottsmedicin, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-68821.
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The results regarding the effects of unaccustomed eccentric exercise on muscle tissue are often conflicting and the aetiology of delayed onset muscle soreness (DOMS) induced by eccentric exercise is still unclear. This study aimed to re-evaluate the paradigm of muscular alterations with regard to muscle sarcolemma integrity and fibre swelling in human muscles after voluntary eccentric exercise leading to DOMS. Ten young males performed eccentric exercise by downstairs running. Biopsies from the soleus muscle were obtained from 6 non-exercising controls, 4 exercised subjects within 1 hour and 6 exercised subjects at 2-3 days and 7-8 days after the exercise. Muscle fibre sarcolemma integrity, infiltration of inflammatory cells and changes in fibre size and fibre phenotype composition as well as capillary supply were examined with specific antibodies using enzyme histochemistry and immunohistochemistry. Although all exercised subjects experienced DOMS which peaked between 1.5 to 2.5 days post exercise, no significant sarcolemma injury or inflammation was detected in any post exercise group. The results do not support the prevailing hypothesis that eccentric exercise causes an initial sarcolemma injury which leads to subsequent inflammation after eccentric exercise. The fibre size was 24% larger at 7-8 days than at 2-3 days post exercise (p<0.05). In contrast, the value of capillary number per fibre area tended to decrease from 2-3 days to 7-8 days post exercise (lower in 5 of the 6 subjects at 7-8 days than at 2-3 days; p<0.05). Thus, the increased fibre size at 7-8 days post exercise was interpreted to reflect fibre swelling. Because the fibre swelling did not appear at the time that DOMS peaked (between 1.5 to 2.5 days post exercise), we concluded that fibre swelling in the soleus muscle is not directly associated with the symptom of DOMS.
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Raue, Ulrika. "Effects of concentric vs eccentric resistance training on skeletal muscle adaptations in humans." Virtual Press, 2001. http://liblink.bsu.edu/uhtbin/catkey/1221284.
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The Beothuk Indians were an extinct group of Amerinds who were among the earliest founders of Newfoundland. In literature, the Beothuk were described as perhaps being phenotypically more similar to Europeans than Asians (Gatschet 1890, Lloyd 1875, 1876a, Marshall 1996). In this research, mitochondrial DNA (mtDNA) analysis was performed on a Beothuk individual in order to determine his haplotype and, perhaps, shed light on the origins of the Beothuk.For this analysis, a tooth of Nonosabasut, a Beothuk chief who died in 1819 was loaned from the Royal Museum of Scotland. Ancient DNA was extracted from 172 mg of dentin from the tooth. The DNA was cut with two blunt-end restriction enzymes, RsaI and HaeIII. Double-stranded DNA adapters were ligated to the blunt ends. A single adapter was used to amplify the resulting fragments using PCR. In this manner, two libraries of the DNA were created that could be readily reamplified using a small amount of the PCR product. mtDNA type was determined by amplifying specific regions and performing Restriction Fragment Length Polymorphism analysis and sequencing. It was determined that the Beothuk individual had a 9-bp deletion at nucleotide position (np) 8272, an Alul restriction site at np 5176, and heteroplasmy for a HincII restriction site at np 13,259, indicating that the Beothuk individual falls into the Native American Haplogroup B. Haplogroup B is not present in modern Siberian populations, whereas the remaining Native American mtDNA haplogroups are. It has been hypothesized that Haplogroup B arrived in the Americas at a different time than haplogroups A, C, D, and X, about 16,000-13,000 YBP (Years Before Present) (Starikovskaya et al. 1998). Haplogroup B can be found in some modern Taiwanese, Japanese, Korean, Evenk, and other Asian populations.Sequencing of the D-Loop region revealed a G to A transition at np 16303. To our knowledge, this transition was never previously reported in a Native American. This transition has been reported in Tibetans, Koreans, Hans, and Japanese, all considered to be southeast Asian Causacoids (Torroni et al. 1993b, 1994b). This transition, also frequently described in the Caucasian Haplogroup H, is especially prevalent in Spain and among the Basque. It is described as a root haplotype of Haplogroup H whose expansion was estimated to be between 12,300-13,200 YBP (Torroni et al. 1998). This time estimate coincides with the expansion of Haplogroup B. One possible explanation for this transition may be some admixture of the Beothuk with a Caucasian population.School of Physical Education
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Jones, Robert. "Critical Roles for Laminin in Skeletal Muscle Morphogenesis and Myotendinous Junction Maintenance." Fogler Library, University of Maine, 2007. http://www.library.umaine.edu/theses/pdf/JonesR2007.pdf.
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Reidy, Paul T. "Influence of aerobic training on skeletal muscle protein composition." CardinalScholar 1.0, 2010. http://liblink.bsu.edu/uhtbin/catkey/1569026.
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Access to abstract permanently restricted to Ball State community onlyAccess to thesis permanently restricted to Ball State community only
School of Physical Education, Sport, and Exercise Science
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Lewis, Trevor M. "Anion pathway in the sarcoplasmic reticulum of skeletal muscle / Trevor M. Lewis." Thesis, Adelaide, S. Aust, 1993. http://hdl.handle.net/2440/21601.
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Raue, Ulrika. "Skeletal muscle gene expression with age." Virtual Press, 2007. http://liblink.bsu.edu/uhtbin/catkey/1370882.
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The aim of this research was to investigate myogenic (i.e. growth) and proteolytic (i.e. breakdown) gene expression (GE) in skeletal muscle of young and old women. Myogenic (MyoD, MRF4, Myf5, myogenin, myostatin) and proteolytic (Atrogin-1, MuRF-1, FOXO3A) genes were examined in the basal state and after resistance exercise (RE). Six old women (OW: 85 ± 1 y) and eight young women (YW: 23 ± 1) performed 3 x 10 knee extensions at 70% of 1-repetition-maximum. Muscle biopsies were obtained from the vastus lateralis (i.e. thigh) before and 4 hours after RE.In the basal state, OW expressed higher levels (p<0.05) of MyoD, MRF4, myf5, myogenin, myostatin, FOXO3A and MuRF-1 compared to YW. Fiber type specific GE analysis in the OW showed that slow-twitch muscle fibers (MHC I) expressed higher levels (p<0.05) of myogenin and Atrogin-1, compared to fast-twitch (MHC Ila) fibers. In response to RE both YW and OW increased (p<0.05) mRNA levels of MyoD and MRF4, while a decrease (p<0.05) was observed for myostatin. MuRF-1 mRNA increased (p<0.05) in both age groups, while there was an age-specific induction (p<0.05) of Atrogin-1 after RE. Fiber type specific GE after RE in the old women showed that MHC Ila fibers did not induce myogenic GE. Robust increases (p<0.05) in MyoD, MRF4, and myogenin were only observed in the MHC I fibers. Both fiber types decreased (p<0.05) myostatin, and increased Atrogin-1 with RE. MuRF-1 mRNA levels increased specifically in MHC Ila fibers. In summary, skeletal muscle of OW expresses higher levels of mRNA for most selected genes at rest. With RE, aging skeletal muscle retains the ability to induce myogenic GE, although exclusive to MHC I fibers. After RE, proteolytic GE induction is greater in OW and most pronounced in MHC Ila fibers. Collectively, these data suggest that an imbalance exists in the regulation of the myogenic and proteolytic program in aging skeletal muscle. This research also provides the first evidence of intrinsic molecular differences between MHC I and MHC Ila fibers in OW, and may, in part, explain the MHC Ila atrophy apparent in sarcopenic muscle.School of Physical Education, Sport, and Exercise Science
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Elashry, Mohamed Ismail Elsayed. "The cellular basis controlling the development of adult skeletal muscles." Thesis, University of Reading, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.553636.
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A major strategy to alleviate myopathic symptoms through enhancing muscle growth and regeneration is to inhibit the action of Myostatin, a TGF -β family member that inhibits muscle growth. Presently however, no study has expanded the morphological analysis of mouse skeletal muscle beyond a few muscles of the hind limb. Therefore I have initially undertaken an expansive analysis of the skeletal musculature of the mouse forelimb and highlighted the species-specific differences with the rat. Subsequently, I examine the musculature of the forelimb in both young and old wild type and Myostatin null mice and assess the potential beneficial effects of Myostatin deletion on muscle morphology and composition with ageing. I show that the mouse muscle displays a more glycolytic phenotype compared to the rat. I demonstrate that in the absence of Myostatin, the induced myofibre hyperplasia (increase in myofibre number), hypertrophy (increase in myofibre size) and glycolytic conversion (fibre type shift towards more glycolytic phenotype) all occur in a muscle-specific manner. Next, I examine the role of Myostatin deletion on the morphology of the nerve axon. I demonstrate that skeletal muscle hyperplasia in Myostatin null mouse is accompanied by an increase in nerve fibres in major nerves of both the fore and hind limb. In addition, I show that axons within these nerves undergo hypertrophy. Furthermore, I provide evidence that the age related neural atrophic process is delayed in the absence of Myostatin. I show that skeletal muscle hyperplasia in the Myostatin null is accompanied by an increase in the number of muscle proprioceptors. Crucially, I demonstrate that absence of Myostatin reduces the amount of the extracellular matrix connective tissue. Furthermore, Myostatin deletion perturbs age-related collagen formation. Finally, I show that lack of Myostatin increases the number and the proliferation potential of satellite cells (skeletal muscle stein cell). Collectively, these data conclude that Myostatin regulates skeletal muscle development.
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Rahman, Mashrur. "Reactive oxygen species mediated regulation of autophagy in skeletal muscles." Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=121322.
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Skeletal muscles comprise of approximately 50% of the human body mass and are critical organs for enabling locomotion and exerting metabolic control. Autophagy, a lysosome-dependant catabolic process involved in the degradation of long-lived proteins and organelles, is an important process responsible for maintaining muscle homeostasis. Reactive Oxygen Species (ROS) has been shown to induce autophagy in many different cell types. In this study, we evaluate the effects of physiological levels of mitochondrial-derived reactive oxygen species (ROS) on skeletal muscle autophagy. In differentiated C2C12 myotubes, basal level autophagy and autophagy triggered by 1.5 to 4 hr of acute nutrient deprivation, inhibition of mTORC1, or leucine deprivation were quantified using a long-lived protein degradation assay (index of proteolysis), LC3B autophagic flux, and mRNA expressions of autophagy-related genes. Pre-incubation with antioxidants tempol (SOD mimetic) or N-acetyl cysteine (NAC) significantly attenuates rates of proteolysis and LC3B flux and blocks increases in acute and nutrient deprivation-, rapamycin treatment- and leucine deprivation-triggered autophagy. Similar results were obtained with mitochondira- specific antioxidants mito-tempol and SS31. MitoSOXTM Red fluorescence measurements confirm that mitochondrial ROS levels increase substantially in response to acute nutrient deprivation and rapamycin treatment and that tempol and mito-tempol attenuates this response. Antioxidants decrease AMPK phosphorylation by 40% and significantly augment AKT phosphorylation, but exert no effects on mTORC1-dependant ULK1 phosphorylation on Ser555. Treatment of mice with NAC significantly attenuated basal LC3B autophagic flux in the diaphragm, confirming that endogenous ROS promotes in vivo muscle autophagy. We report for the first time that mitochondrial-derived ROS promote skeletal muscle autophagy and that this effect is mediated in part through AKT inhibition and autophagy initiation via AMPK activation.Les muscles squelettiques constituent environ 50% de la masse du corps humain et représente un organe essentiel permettant la locomotion et le contrôle métabolique. L'autophagie, un processus catabolique lysosome-dépendant, est impliquée dans la dégradation des protéines et des organites à long terme. Elle représente un processus important pour le maintien de l'homéostasie du muscle. Par ailleurs, il a été montré que les radicaux libres (ROS) principalement générés par les mitochondries, induisent l'autophagie dans de nombreux types cellulaires. Dans cette étude, nous voulons évaluer des radicaux libres mitochondriaux (ROS) à un niveau physiologique sur l'autophagie dans le muscle squelettiqueDans les myotubes différenciés C2C12, le niveau basal de l'autophagie et son activation (déclenchées par 1,5 à 4 h de carence aigüe en nutriments, par l'inhibition de mTORC1, ou encore par la privation en leucine) ont été quantifiés à l'aide d'un test de longue durée de dégradation des protéines (indice de protéolyse), par le flux d'autophagie LC3B, ou par les l'ARNm des gènes liés à l'autophagie. La pré-incubation avec des antioxydants de type tempol (SOD mimétique) ou N-acétylcystéine (NAC) atténue considérablement les niveaux de protéolyse, de flux de LC3B et bloque l'activation de l'autophagie secondaire à la carence en nutriments –traitement par rapamycine- ou la carence en leucine. Des résultats similaires ont été obtenus avec es antioxydants spécifiques de la mitochondrie mito-tempol et SS31. Des mesures de fluorescence rouge MitoSOXTM confirment que le niveau de radicaux libres mitochondriaux augmentent considérablement en réponse à une carence en nutriments aiguë ou au traitement par rapamycine et que le tempol et mito-tempol atténue cette réponse. Les antioxydants entraîne une diminution de 40% de la phosphorylation de l'AMPK et augmente significativement la phosphorylation de l'AKT, mais sans exercer aucun effet sur mTORC1 qui est dépendant de la phosphorylation sur Ser555 ULK1. Le traitement des souris avec NAC atténue significativement le flux autophagique basal de LC3B dans le diaphragme, ce qui confirme que les ROS endogènes favorise l'autophagie musculaire in vivo.Nous rapportons pour la première fois que les ROS mitochondriaux sont responsable de l'activation de l'autophagie dans le muscle squelettique et que cet effet est médié en partie par l'inhibition de AKT et de l'initiation de l'autophagie par activation de l'AMPK.
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Morton, Alison J. "Adaptive growth of uterine and skeletal muscles in the rat." Thesis, Queen's University Belfast, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.329343.
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Ballard, H. J. "Adenosine release and vascular responses in contracting dog skeletal muscles." Thesis, University of Leeds, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.355698.
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Liang, Jingjing. "Toxicity and Processing of Cellular Prion Protein in Skeletal Muscles." Case Western Reserve University School of Graduate Studies / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=case1323450797.
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Alshammari, Abdullah A. A. M. F. "Mathematical modelling of oxygen transport in skeletal and cardiac muscles." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:65a34cb0-ef00-44c9-a04d-4147844c76ac.
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Understanding and characterising the diffusive transport of capillary oxygen and nutrients in striated muscles is key to assessing angiogenesis and investigating the efficacy of experimental and therapeutic interventions for numerous pathological conditions, such as chronic ischaemia. In articular, the influence of both muscle tissue and microvascular heterogeneities on capillary oxygen supply is poorly understood. The objective of this thesis is to develop mathematical and computational modelling frameworks for the purpose of extending and generalising the current use of histology in estimating the regions of tissue supplied by individual capillaries to facilitate the exploration of functional capillary oxygen supply in striated muscles. In particular, we aim to investigate the balance between local capillary supply of oxygen and oxygen demand in the presence of various anatomical and functional heterogeneities, by capturing tissue details from histological imaging and estimating or predicting regions of capillary supply. Our computational method throughout is based on a finite element framework that captures the anatomical details of tissue cross sections. In Chapter 1 we introduce the problem. In Chapter 2 we develop a theoretical model to describe oxygen transport from capillaries to uniform muscle tissues (e.g. cardiac muscle). Transport is then explored in terms of oxygen levels and capillary supply regions. In Chapter 3 we extend this modelling framework to explore the influence of the surrounding tissue by accounting for the spatial anisotropies of fibre oxygen demand and diffusivity and the heterogeneity in fibre size and shape, as exemplified by mixed muscle tissues (e.g. skeletal muscle). We additionally explore the effects of diffusion through the interstitium, facilitated--diffusion by myoglobin, and Michaelis--Menten kinetics of tissue oxygen consumption. In Chapter 4, a further extension is pursued to account for intracellular heterogeneities in mitochondrial distribution and diffusive parameters. As a demonstration of the potential of the models derived in Chapters 2--4, in Chapter 5 we simulate oxygen transport in myocardial tissue biopsies from rats with either impaired angiogenesis or impaired arteriolar perfusion. Quantitative predictions are made to help explain and support experimental measurements of cardiac performance and metabolism. In the final chapter we summarize the main results and indicate directions for further work.
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Kohn, Tertius A. "Characteristics and adaptation of skeletal muscle to endurance exercise." Thesis, Stellenbosch : University of Stellenbosch, 2011. http://hdl.handle.net/10019.1/16517.
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Thesis (PhD)--University of Stellenbosch, 2005.ENGLISH ABSTRACT: Skeletal muscle adapts to stimuli by modifying structural and metabolic protein expression. Furthermore, a muscle group may vary within itself to accommodate specialisation in regions. Structural and metabolic characteristics of an individual are regulated partly by genotype, but contraction duration and intensity may play a greater role in muscle phenotype. The aims of this dissertation were to investigate: structural and metabolic regionalisation in a muscle group, possible relationships between training volume and intensity and hybrid fibres, muscle characteristics of athletes from two different ethnic groups, and muscle adaptation in already well-trained athletes subjected to high intensity interval training. Myosin heavy chain (MHC) isoform content and citrate synthase (CS) activities were measured in the Quadriceps femoris (QF) muscle of 18 female rats. Muscle was divided into superficial, middle and deep, distal, central and proximal parts. MHC IIb and IIx were more abundant in superficial regions (P < 0.05) with low CS activities compared to deeper parts. Isoform content varied along the length of deep regions. This study showed that the QF has regional specialisation. Therefore, standardisation of sampling site is important. Hybrid fibre proportions in muscle biopsies of 12 middle distance runners and 12 non-runners were investigated. MHC IIa/IIx correlated with training volume/week in runners (r = -0.66, P < 0.05) and MHC IIa/IIx correlated with exercise hours/week in non-runners (r = -0.72, P < 0.01). Average preferred racing distance (PRDA) correlated better with MHC IIa/IIx in runners (r = -0.85, P < 0.001). MHC IIa/IIx may therefore be more closely related to exercise intensity than previously thought. Fibre type characteristics and performance markers were investigated in 13 Xhosa and 13 Caucasian distance runners, matched for performance, training volume and PRDA. Xhosa runners had less MHC I and more MHC IIa fibres in muscle biopsies than Caucasian runners (P < 0.05). Xhosa runners had lower plasma lactate at 80% peak treadmill speed (PTS) (P < 0.05), but higher lactate dehydrogenase (LDH) (P < 0.01) and phosphofructokinase (P = 0.07) activities in homogenate muscle samples. LDH activities in MHC I (P = 0.05) and IIa (P < 0.05) fibre pools were higher in Xhosa runners. Xhosa athletes may thus have a genetic advantage or they may have adapted to running at a higher intensity. Six weeks of individually standardised high intensity interval treadmill training (HIIT) were investigated in 15 well-trained runners. PTS increased after HIIT (P < 0.01), while maximum oxygen consumption (VO2max) only showed a tendency to have increased as a result of HIIT (P = 0.06). Sub-maximal tests showed lower plasma lactate at 64% PTS (P = 0.06), with lower heart rates at workloads from 64% to 80% PTS (P < 0.01) after HIIT. No changes were observed for cross-sectional area, capillary supply and enzyme activities in homogenates muscle samples. LDH activity showed a trend (P = 0.06) to have increased in MHC IIa pools after HIIT. Higher HIIT speed was related to decreases in MHC I fibres, but increases in MHC IIa/IIx fibres (r = -0.70 and r = 0.68, respectively, P < 0.05). Therefore, HIIT may alter muscle fibre composition in well-trained runners, with a concomitant improvement in performance markers.
AFRIKAANSE OPSOMMING: Skeletspier kan adapteer deur strukturele en metaboliese protein ekspressie te verander as gevolg van stimulante. ‘n Spiergroep kan ook intern verskil om spesialisering in spierdele toe te laat. Strukturele en metaboliese karaktereienskappe van ‘n individu word deels gereguleer deur gene, maar kontraksie tydperk en intensiteit mag ‘n groter rol speel in spierfenotipe. Die doelwitte van hierdie tesis was om ondersoek in te stel in: strukturele en metaboliese eienskappe in spiergroepstreke, moontlike verhoudings tussen oefeningsvolume of intensiteit en baster vesels, spier eienskappe in atlete van twee etniese groepe, en spier adaptasie in goed geoefende atlete blootgestel aan hoë intensiteit interval oefening. Miosien swaar ketting (MSK) isovorm inhoud en sitraat sintase (SS) aktiwiteite is gemeet in die Quadriceps femoris (QF) spier van 18 wyfie rotte. Spiere was opgedeel in oppervlakkig, middel en diep, asook distaal, sentraal en proksimale dele. MSK IIb en IIx was meer oorvloedig in oppervlakkige dele (P < 0.05) met lae SS aktiwiteite in vergelyking met dieper dele. Isovorm inhoud het ook verskil oor die lengte van diep dele. Dus bevat die QF gespesialiseerde streke en is die area van monsterneming belangrik. Baster vesel proporsies is ondersoek in spiermonsters van 12 middel afstand hardlopers en 12 niehardlopers. MSK IIa/IIx van hardlopers het met oefeningsvolume/week gekorreleer (r = -0.66, P < 0.05), asook MSK IIa/IIx van nie-hardlopers met oefeningsure/week (r = -0.72, P < 0.01). Gemiddelde voorkeur wedloop afstand (VWAG) het beter met MSK IIa/IIx gekorreleer in hardlopers (r = -0.85, P < 0.001). MSK IIa/IIx mag dus meer verwant wees aan oefeningsintensiteit. Veseltipe eienskappe en prestasie merkers was ondersoek in 13 Xhosa en 13 Caucasian langafstand atlete, geëweknie vir prestasie, oefeningsvolume en VMAG. Xhosa hardlopers het minder tipe I en meer tipe IIA vesels in hul spiermonsters gehad as die Caucasian hardlopers (P < 0.05). Xhosa hardlopers het laer plasma laktaat by 80% van hul maksimale trapmeul spoed (MTS) (P < 0.05), maar hoër laktaat dihidrogenase (LDH) (P < 0.01) en fosfofruktokinase (P = 0.07) aktiwiteite in homogene spiermonsters gehad. LDH aktiwiteite in MSK I (P = 0.05) en IIa (P < 0.05) veselbondels was hoër in Xhosa hardlopers. Xhosa atlete mag dus ‘n genetiese voorsprong geniet, of hulle het geadapteer om by hoër intensiteite te hardloop. Ses weke van geïndividualiseerde gestandardiseerde hoë intensiteit interval trapmeul oefening (HIIT) was ondersoek in 15 goed geoefende hardlopers. MTS het verhoog na HIIT (P < 0.01), en maksimale surrstof verbruik (VO2max) het ‘n neiging getoon om te verhoog het na HIIT (P = 0.07). Submaksimale toetse het laer plasma laktaat by 64% MTS getoon (P = 0.06), met laer harttempos by werkladings 64% tot 80% MTS (P < 0.01). Geen veranderings was gemerk vir deursnit area, kapillêre toevoer en ensiem aktiwiteite in homogene spiermonsters nie. LDH aktiwiteit het ‘n neiging getoon om te verhoog het (P = 0.06) in MSK IIa veselbondels na HIIT. Hoër HIIT snelhede was verwant aan ‘n daling in MSK I vesels, maar ‘n verhoging in MSK IIa/IIx vesels (r = -0.70 en r = 0.68, respektiwelik, P < 0.05). HIIT mag dus spier veseltipe verander in goed geoefende hardlopers, met gevolglike verbetering in prestasie merkers.
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Vlahovich, Nicole. "The role of cytoskeletal tropomyosins in skeletal muscle and muscle disease." View thesis, 2007. http://handle.uws.edu.au:8081/1959.7/32176.
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Thesis (Ph.D.)--University of Western Sydney, 2007.A thesis presented to the University of Western Sydney, College of Health and Science, School of Natural Sciences, in fulfilment of the requirements for the degree of Doctor of Philosophy. Includes bibliographies.
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Banas, Krystyna Anna. "K(ATP) channel Kir62 subunit distribution differs between muscles and between fiber types in skeletal muscle." Thesis, University of Ottawa (Canada), 2010. http://hdl.handle.net/10393/28483.
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The activity of the ATP-sensitive potassium (KATP) channel, whose sensitivity to ATP and ability to permit K+ flux together allow the channel to couple the metabolic state of a cell to its membrane excitability, is important in several tissues for the maintenance of glucose homeostasis and cytoprotection. In skeletal muscle specifically, the channel has been shown to be involved in cell volume regulation, modulation of glucose uptake, and the prevention of fiber damage and contractile dysfunction during fatigue. The extent of the cytoprotective capabilities of the KATP channel vary tremendously between muscles with different muscle fiber type composition. Semi-quantitative measurement of Kir6.2 subunit content showed that variances exist in KATP channel content between fiber types and between different muscles. These differences may be related to the extent of importance of the channel's function in a specific muscle. The highest Kir6.2 content was observed in the most glycolytic fiber types and in the more glycolytic muscles studied, and it is these muscles and fiber types which appear to be most dependent on functional KATP channels for their cytoprotective role.
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Satarug, Soisungwan. "Responses of skeletal muscle protein turnover and amino acid concentration to unloading, denervation and immobilization." Diss., The University of Arizona, 1987. http://hdl.handle.net/10150/184308.
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The effects of denervation, non-weight bearing (unloading) or immobilization on hindlimb muscle growth, protein and amino acid metabolism were studied. In the first 3 days after denervation or unloading, atrophy of the soleus was caused by a suppression of protein synthesis and an acceleration of protein degradation. Thereafter, further atrophy, up to 6 days was due to depressed protein synthesis only. The changes in both protein synthesis and degradation in the first three days accounted for 69% and 65%, respectively, of the total loss of protein and mass in 6 days of unloaded or denervated soleus. Over the 6-day period, denervated soleus lost more mass and protein than the unloaded muscle owing to the earlier onset and greater extent of proteolysis. In denervated soleus, both lysosomal and non-lysosomal proteolysis may be enhanced, whereas in the unloaded muscle possibly only non-lysosomal proteolysis was enhanced. In both cases non-lysosomal proteolysis may be mediated by Ca²⁺-activated neutral protease, partially as a result of Ca²⁺ release from sarcoplasmic reticulum. Possibly due to the lack of lysosomal proteolysis, the insulin receptor did not show apparent increased turnover with unloading, as suggested by increased insulin sensitivity of in vitro protein turnover in the unloaded soleus. In contrast, denervated soleus showed a normal response to insulin for in vitro protein turnover. These findings suggested a mechanistic difference of unloading and denervation atrophy of soleus. A decreased ratio of glutamine/glutamate in fresh muscle suggested that the synthesis of glutamine in soleus may be diminished by denervation just as by unloading. This diminution of glutamine synthesis was probably due to reduced availability of ammonia, as evidenced by the slow disappearance of ATP in incubated denervated soleus. Similiar to unloading, denervation led to a decrease in aspartate concentration. This decreased concentration apparently resulted in decreased rather than increased utilization of aspartate. Effects of stretch on unloaded soleus were particularly pronounced in the first two days. Thereafter, in the stretched, unloaded soleus protein degradation increased to nearly the same extent as did protein synthesis. Hence after two days, stretch seems to lose its effectiveness in mitigating the effects of unloading so that it may not be an adequate preventive measure of muscle wasting under non-weight bearing condition.
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Scionti, Isabella. "Epigenetic Regulation of Skeletal Muscle Differentiation." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSEN084/document.
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LSD1 et PHF2 sont des déméthylases de lysines capables de déméthyler à la fois les protéines histones qui influencent l’expression génique et les protéines non histones en affectant leurs activités ou stabilités. Des approches fonctionnelles d’inactivation de Lsd1 ou Phf2 chez la souris ont démontré l’implication de ces enzymes dans l'engagement des cellules progénitrices au cours de la différenciation. La myogenèse est l'un des exemples les mieux caractérisés sur la façon dont les cellules progénitrices se multiplient et se différencient pour former un organe fonctionnel. Elle est initiée par une expression temporelle spécifique des gènes régulateurs cibles. Parmi ces facteurs, MYOD est un régulateur clé de l'engagement dans la différenciation des cellules progénitrices musculaires. Bien que l’action de MYOD au cours de la différenciation cellulaire ait été largement étudiée, peu de chose sont connus sur les événements de remodelage de la chromatine associés à l'activation de l'expression de MyoD. Parmi les régions régulatrices de l'expression de MyoD, la région Core Enhancer (CE) qui est transcrite en ARN activateur non codant (CEeRNA) a été démontrée pour contrôler l'initiation de l'expression de MyoD au cours de l'engagement de myoblastes dans la différenciation.Nous avons identifié LSD1 et PHF2 comme des activateurs clés du CE de MyoD. L'invalidation in vitro et in vivo de LSD1 ou l'inhibition de l'activité enzymatique de LSD1 empêche le recrutement de l'ARN PolII sur le CE, empêchant l’expression du CEeRNA. D’après nos résultats, l'expression forcée du CEeRNA restaure efficacement l'expression de MyoD et la fusion myoblastique en l'absence de LSD1. De plus, PHF2 interagit avec LSD1 en régulant sa stabilité protéique.En effet, l'ablation in vitro de PHF2 entraîne une dégradation massive de LSD1 et donc une absence d'expression du CEeRNA. Cependant, toutes les modifications d'histones qui ont lieu dans la région du CE lors de l'activation de la différenciation ne peuvent pas être directement attribuées à l'activité enzymatique de LSD1 ou PHF2. Ces résultats soulèvent la question de l'identité des partenaires de LSD1 et PHF2, qui co-participeraient à l'expression du CEeRNA et donc à l'engagement des myoblastes dans la différenciation cellulaireLSD1 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
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Holtermann, Andreas. "Inhomogeneous activation of skeletal muscles. Investigated by multi-channel surface electromyography." Doctoral thesis, Norwegian University of Science and Technology, Department of Social Work and Health Science, 2008. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-2111.
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Background
The current understanding of neuromuscular control is based on the related characteristics of the motoneuron (size) and its belonging muscle fibers resulting in a stereotyped activation of all motor units within a muscle. This “size principle” was originally founded on the anatomical and histochemical non-complex soleus muscle of decerebrated cats. However, deviations from this stereotyped control are observed during voluntary contractions in anatomical complex muscles. The main objective of this thesis was to investigate intra-muscular spatial dependency of activation, control and physiological characteristics of the anatomical complex biceps brachii and trapezius muscle with a multi-channel surface electromyographical (MCsEMG) technique.
Methods
MCsEMG recordings from the biceps brachii and the trapezius muscle were performed during isometric slow force modulation and sustained sub-maximal contractions. The applied MCsEMG grid consists of 13 by 10 surface electrodes covering 6 x 4.5 cm of the skin surface. To obtain information about recruitment of motor unit populations from a large fraction of the muscles, changes in spatial distribution of activity with force modulation and fatigue were quantified by correlating the root-mean-square amplitude from all electrodes at different time-epochs within and between contraction types. Frequency and duration of repeated shifts in activity between intra-muscular regions (differential activation) were investigated by calculating the average activity level from (electrodes situated above) the two heads of the biceps brachii, respectively, throughout a sustained sub-maximal contraction until exhaustion. To examine the distribution of common synaptic input to motoneurons innervating the biceps brachii with fatigue, a descriptor for motor unit synchronization was quantified based on changes in the monopolar MCsEMG signals during a sustained contraction. To attain in vivo information about intra-muscular distribution of physiological characteristics, the muscle fiber conduction velocity and fiber orientation were estimated based on detection of propagating motor unit action potentials from large fractions of the biceps brachii and the upper trapezius muscle with the MCsEMG technique.
Main findings and conclusions
The biceps brachii and the trapezius muscle were inhomogeneously activated during force regulation and fatigue due to recruitment of differently located motor units within the muscles. The changes in spatial distribution of biceps brachii activity with force gradation were consistent within and between subjects, indicating that changes in spatial distribution of intra-muscular activity are suited to attain information about recruitment of motor unit populations. The changes in spatial distribution of upper trapezius activity were similar during sustained and ramp contractions, indicating an orderly recruitment sequence of motor unit populations during sustained contractions. The regions (long and short head) of the biceps brachii were differentially activated during a sustained contraction, indicating a partially selective control of intra-muscular regions. However, this region-dependent activation of the biceps brachii muscle was not associated with time to exhaustion at a contraction level of 25 % of maximal voluntary contraction. The motor unit synchronization descriptor was different between regions within the biceps brachii muscle with fatigue, indicating an uneven distribution of common synaptic input to the motoneurons of the muscle. Consistent with studies of human cadavers, the muscle fiber characteristics were dependent on the intra-muscular regions of the upper trapezius muscle. The findings from this thesis support an intramuscular spatial dependency of the activation, control and physiological characteristics of the biceps brachii and the trapezius muscle.
Paper I, IV and V reproduced with kind permission of Elsevier, sciencedirect.com
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Yang, Hairu. "Drosophila skeletal muscles regulate the cellular immune response against wasp infection." Doctoral thesis, Umeå universitet, Institutionen för molekylärbiologi (Medicinska fakulteten), 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-125842.
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Drosophila melanogaster is widely used as a model organism to study the innate immune system because it lacks an adaptive immune response that could mask its innate immune response. The innate immune response of Drosophila primarily consists of humoral and cellular immune responses. The humoral immune response ismediated by antimicrobial peptides, and is induced by bacterial and fungal infections. The cellular immune response is mediated by blood cells (hemocytes), and is induced by bacterial and wasp infection. While the humoral immune response of Drosophila has been studied extensively, the cellular immune response is less well understood. In this work, I investigated the communication between different signaling pathways and tissues in Drosophila during infection by the parasitic wasp Leptopilina boulardi. I find that JAK/STAT signaling is strongly activated by wasp infection, in both hemocytes and (unexpectedly) larval skeletal muscles. This activation is mediated by the cytokines Upd2 and Upd3, which are secreted from circulating hemocytes. Deletion of upd2 or/and upd3 weakens the wasp-induced activation of JAK/STAT signaling in skeletal muscles and the cellular immune response to wasp infection, leading to reduced encapsulation of wasp eggs and a decrease in the number of circulating lamelloyctes. The suppression of JAK/STAT signaling also significantly weakens the cellular immune response in skeletal muscles, but not in fat bodies and hemocytes. However, the activation of this signaling in skeletal muscles has no obvious effect on the cellular immune response. Together, these results suggest that rather than being uninvolved bystanders, Drosophila skeletal musclesactively participate in cellular immune responses against wasp infection. To answer how Drosophila larval muscles participate cellular immune response, I min-screened the effects of several immune related signaling pathways in the muscles and the fat body on the cellular immune response. Interestingly, the cellular immune response was only significantly compromised by the suppression ofinsulin signaling in skeletal muscles, in a way that was veryreminiscent of the phenotypes induced by suppressing JAK/STAT signaling in muscles. While wasp infection activates JAK/STAT signaling in muscles, it has the opposite effect on insulin signaling. In addition, I find that insulin signaling in skeletal muscles can positively regulate JAK/STAT signaling. On the other hand, suppression of JAK/STAT signaling in muscles reduces insulin signaling locally in muscles and systemically in the fat body. Suppression of either insulin or JAK/STAT signaling in muscles leads to reductions in glycogen storage in muscles, the trehalose concentration in the hemolymph, and the frequency of feeding behavior. All these results indicate that JAK/STAT and insulin signaling in Drosophila skeletal muscles regulate cellular immune responses via their effects on carbohydrate metabolism. Our findings shed new light on the interactions between diabetes, metabolism, the immune system, and tissue communication.
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Trappe, Todd A. "Skeletal muscle and cardiorespiratory responses to simulated microgravity." Virtual Press, 1996. http://liblink.bsu.edu/uhtbin/catkey/1018783.
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As a part of a project designed to mimic a Space Shuttle flight (LMS), eight healthy males completed 17 d of -6° head down tilt bedrest to assess the in vivo torque velocity relationship of the calf muscle group and the cardiorespiratory responses to supine cycling exercise. The subjects age, height, and weight were 42.7 ±8.1 y, 182.3 ±6.5 cm, and 82.2 ±12.1 kg, respectively. Testing was completed prior to bedrest (CON), on bedrest days 2 & 3 (BR 1), 8 & 9 (BR2), and 13 & 14 (BR3), as well as recovery days 3 & 4 (R1), and 7 & 8 (R2). Maximal plantar flexion force production at seven angular velocities (0, 30, 60, 120, 180, 240, 300'- s-1) was unchanged (P>0.05) during bedrest and recovery. Muscle biopsy specimens obtained from the soleus before and on day 17 of bedrest showed no change (P>0.05) in muscle fiber composition, muscle fiber area, capillary to fiber ratio, or capillary density. Citrate synthase activity decreased 21% (P<0.05) from 122.1 ±7.8 to '97.1 ±5.1 µmol -min-1 • g dry wt-1, while phosphorylase activity was unchanged (P>0.05). VO2max (L • min-1) was decreased (P<0.05) from CON (3.24 ±0.20) during BR1 (2.99 ±0.17; -7.3%), BR2 (3.00 ±0.17; -7.1%), BR3 (2.92 ±0.20; -9.0%), and R1 (3.02 ±0.20; -6.6%), but was not different (P>0.05) than CON by R2 (3.13 ±0.19; -3.3%). Maximal heart rate and ventilation did not change (P>0.05) from CON during bedrest or recovery. Initial changes in VO2max (BR1) were significantly correlated with fluid balance during bedrest day 1 (r=0.91, P<0.05). These data suggest that the testing protocols in this investigation may be sufficient to attenuate functionally significant changes in muscle morphology and strength during 17 d of simulated microgravity. The results also suggest that the time course for changes in VO2max are not linear and are related to the initial changes in body fluid volumes.Human Performance Laboratory
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Rathbone, Christopher R. "Mechanisms regulating skeletal muscle satellite cell cycle progression." Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/5866.
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Thesis (Ph. D.)--University of Missouri-Columbia, 2006.The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "December 2006" Includes bibliographical references.