Relevant bibliographies by topics / Skeletal and cardiac muscle

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Skeletal and cardiac muscle'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Skeletal and cardiac muscle"

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Minami, Elina, Hans Reinecke, and Charles E. Murry. "Skeletal muscle meets cardiac muscle." Journal of the American College of Cardiology 41, no. 7 (2003): 1084–86. http://dx.doi.org/10.1016/s0735-1097(03)00083-4.

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Zhang, Tan, Xin Feng, Bo Feng, et al. "CARDIAC TROPONIN T MEDIATED AUTOIMMUNE RESPONSE AND ITS ROLE IN SKELETAL MUSCLE AGING." Innovation in Aging 3, Supplement_1 (2019): S882. http://dx.doi.org/10.1093/geroni/igz038.3231.

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Abstract Cardiac troponin T (cTnT), a key component of contractile machinery essential for muscle contraction, is also expressed in skeletal muscle under certain conditions (e.g. neuromuscular diseases and aging). We have reported that skeletal muscle cTnT regulates neuromuscular junction denervation preferentially in fast skeletal muscle of old mice. Here, we further report that cTnT is also enriched within some myofibers, and/or along microvascular walls in old mice fast skeletal muscle. Strikingly, immunoglobulin G (IgG), together with markers of complement system activation, cell death (necroptosis or apoptosis), and macrophage infiltration, were all found to be co-localized with cTnT and IgG in those areas. In addition, elevated cTnT and IgG are associated with lower dystrophin expression on muscle fiber membrane, lower muscle capillary density, and reduced muscle performance (wire hanging test). Using purified recombinant TnT proteins, we confirmed that only cTnT, but not slow or fast skeletal muscle TnT1 or TnT3, was detected by immunoblot using sera from old (but not young) mice with pre-determined elevated cTnT and IgG in their skeletal muscle, indicating the existence of anti-cTnT autoantibodies in sera (previously found in human blood) and skeletal muscle of old mice. Immunoblotting further revealed that the age related changes in skeletaI muscle cTnT and IgG are more prominent in fast skeletal muscle than in slow. Importantly, elevated cTnT and IgG were also detected in skeletal muscles from 4 older adults (65-70 yrs, IMFIT). Our finding suggests a novel autoimmune mechanism mediated by cTnT that underlies age related skeletal muscle abnormalities and dysfunction.
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Park, Song-Young, Jayson R. Gifford, Robert H. I. Andtbacka, et al. "Cardiac, skeletal, and smooth muscle mitochondrial respiration: are all mitochondria created equal?" American Journal of Physiology-Heart and Circulatory Physiology 307, no. 3 (2014): H346—H352. http://dx.doi.org/10.1152/ajpheart.00227.2014.

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Unlike cardiac and skeletal muscle, little is known about vascular smooth muscle mitochondrial respiration. Therefore, the present study examined mitochondrial respiratory rates in smooth muscle of healthy human feed arteries and compared with that of healthy cardiac and skeletal muscles. Cardiac, skeletal, and smooth muscles were harvested from a total of 22 subjects (53 ± 6 yr), and mitochondrial respiration was assessed in permeabilized fibers. Complex I + II, state 3 respiration, an index of oxidative phosphorylation capacity, fell progressively from cardiac to skeletal to smooth muscles (54 ± 1, 39 ± 4, and 15 ± 1 pmol·s−1·mg−1, P < 0.05, respectively). Citrate synthase (CS) activity, an index of mitochondrial density, also fell progressively from cardiac to skeletal to smooth muscles (222 ± 13, 115 ± 2, and 48 ± 2 μmol·g−1·min−1, P < 0.05, respectively). Thus, when respiration rates were normalized by CS (respiration per mitochondrial content), oxidative phosphorylation capacity was no longer different between the three muscle types. Interestingly, complex I state 2 normalized for CS activity, an index of nonphosphorylating respiration per mitochondrial content, increased progressively from cardiac to skeletal to smooth muscles, such that the respiratory control ratio, state 3/state 2 respiration, fell progressively from cardiac to skeletal to smooth muscles (5.3 ± 0.7, 3.2 ± 0.4, and 1.6 ± 0.3 pmol·s−1·mg−1, P < 0.05, respectively). Thus, although oxidative phosphorylation capacity per mitochondrial content in cardiac, skeletal, and smooth muscles suggest all mitochondria are created equal, the contrasting respiratory control ratio and nonphosphorylating respiration highlight the existence of intrinsic functional differences between these muscle mitochondria. This likely influences the efficiency of oxidative phosphorylation and could potentially alter ROS production.
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Herring, B. P., M. H. Nunnally, P. J. Gallagher, and J. T. Stull. "Molecular characterization of rat skeletal muscle myosin light chain kinase." American Journal of Physiology-Cell Physiology 256, no. 2 (1989): C399—C404. http://dx.doi.org/10.1152/ajpcell.1989.256.2.c399.

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A 1.85-kilobase (kb) cDNA has been isolated that encodes the catalytic and calmodulin binding domains of rat skeletal muscle myosin light chain kinase. The cDNA hybridized to a 3.3-kb RNA present in fast- and slow-twitch skeletal muscles. The reported enzymatic activity (3-fold greater in fast- than slow-twitch skeletal muscles) reflects the relative abundance of this RNA in the two types of skeletal muscle. No hybridization of the cDNA was detected to RNA isolated from smooth or nonmuscle tissues. The clone cross hybridized to a 2.2-kb RNA present in cardiac tissue. Ribonuclease protection analysis of skeletal and cardiac muscle RNA revealed major differences in the two hybridizing RNAs. Thus rat skeletal muscle contains a single myosin light chain kinase isoform, which is distinct from the cardiac, smooth, and nonmuscle forms.
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Hooper, Timothy L., and Larry W. Stephenson. "Skeletal muscle for cardiac assistance." Current Opinion in Cardiology 6, no. 2 (1991): 263–68. http://dx.doi.org/10.1097/00001573-199104000-00013.

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Letsou, George V., John H. Braxton, John A. Elefteriades, and Stephan Ariyan. "Skeletal Muscle for Cardiac Assist." Cardiology Clinics 13, no. 1 (1995): 125–35. http://dx.doi.org/10.1016/s0733-8651(18)30069-9.

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Lim, Megan S., and Michael P. Walsh. "Phosphorylation of skeletal and cardiac muscle C-proteins by the catalytic subunit of cAMP-dependent protein kinase." Biochemistry and Cell Biology 64, no. 7 (1986): 622–30. http://dx.doi.org/10.1139/o86-086.

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Catecholamines are known to influence the contractility of cardiac and skeletal muscles, presumably via cAMP-dependent phosphorylation of specific proteins. We have investigated the in vitro phosphorylation of myofibrillar proteins by the catalytic subunit of cAMP-dependent protein kinase of fast- and slow-twitch skeletal muscles and cardiac muscle with a view to gaining a better understanding of the biochemical basis of catecholamine effects on striated muscles. Incubation of canine red skeletal myofibrils with the isolated catalytic subunit of cAMP-dependent protein kinase and Mg-[γ-32P]ATP led to the rapid incorporation of [32P]phosphate into five major protein substrates of subunit molecular weights (MWs) 143 000, 60 000, 42 000, 33 000, and 11 000. The 143 000 MW substrate was identified as C-protein; the 42 000 MW substrate is probably actin; the 33 000 MW substrate was shown not to be a subunit of tropomyosin and, like the 60 000 and 11 000 MW substrates, is an unidentified myofibrillar protein. Isolated canine red skeletal muscle C-protein was phosphorylated to the extent of ~0.5 mol Pi/mol C-protein. Rabbit white skeletal muscle and bovine cardiac muscle C-proteins were also phosphorylated by the catalytic subunit of cAMP-dependent protein kinase, both in myofibrils and in the isolated state. Cardiac C-protein was phosphorylated to the extent of 5–6 mol Pi/mol C-protein, whereas rabbit white skeletal muscle C-protein was phosphorylated at the level of ~0.5 mol Pi/mol C-protein. As demonstrated earlier by others, C-protein of skeletal and cardiac muscles inhibited the actin-activated myosin Mg2+-ATPase activity at low ionic strength in a system reconstituted from the purified skeletal muscle contractile proteins (actin and myosin). Phosphorylation of skeletal or cardiac C-proteins had no effect on their inhibition of this actomyosin Mg2+-ATPase activity. Furthermore, cardiac C-protein inhibited the Mg2+-ATPase activity of desensitized cardiac actomyosin; in this case, phosphorylation of cardiac C-protein enhanced its inhibitory effect on the actomyosin Mg2+-ATPase. These observations suggest that C-proteins of fast- and slow-twitch skeletal muscle fibers and cardiac muscle fibers are phosphorylated in response to catecholamines and other agents which induce cAMP formation and that, at least in the heart, this phosphorylation may affect actin–myosin interaction and the contractile state of the muscle.
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Shiina, Takahiko, Takeshi Shima, Kazuaki Masuda, et al. "Contractile Properties of Esophageal Striated Muscle: Comparison with Cardiac and Skeletal Muscles in Rats." Journal of Biomedicine and Biotechnology 2010 (2010): 1–7. http://dx.doi.org/10.1155/2010/459789.

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The external muscle layer of the mammalian esophagus consists of striated muscles. We investigated the contractile properties of esophageal striated muscle by comparison with those of skeletal and cardiac muscles. Electrical field stimulation with single pulses evoked twitch-like contractile responses in esophageal muscle, similar to those in skeletal muscle in duration and similar to those in cardiac muscle in amplitude. The contractions of esophageal muscle were not affected by an inhibitor of gap junctions. Contractile responses induced by high potassium or caffeine in esophageal muscle were analogous to those in skeletal muscle. High-frequency stimulation induced a transient summation of contractions followed by sustained contractions with amplitudes similar to those of twitch-like contractions, although a large summation was observed in skeletal muscle. The results demonstrate that esophageal muscle has properties similar but not identical to those of skeletal muscle and that some specific properties may be beneficial for esophageal peristalsis.
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Tchao, Jason, Jong Jin Kim, Bo Lin, et al. "Engineered Human Muscle Tissue from Skeletal Muscle Derived Stem Cells and Induced Pluripotent Stem Cell Derived Cardiac Cells." International Journal of Tissue Engineering 2013 (December 5, 2013): 1–15. http://dx.doi.org/10.1155/2013/198762.

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During development, cardiac and skeletal muscle share major transcription factors and sarcomere proteins which were generally regarded as specific to either cardiac or skeletal muscle but not both in terminally differentiated adult cardiac or skeletal muscle. Here, we investigated whether artificial muscle constructed from human skeletal muscle derived stem cells (MDSCs) recapitulates developmental similarities between cardiac and skeletal muscle. We constructed 3-dimensional collagen-based engineered muscle tissue (EMT) using MDSCs (MDSC-EMT) and compared the biochemical and contractile properties with EMT using induced pluripotent stem (iPS) cell-derived cardiac cells (iPS-EMT). Both MDSC-EMT and iPS-EMT expressed cardiac specific troponins, fast skeletal muscle myosin heavy chain, and connexin-43 mimicking developing cardiac or skeletal muscle. At the transcriptional level, MDSC-EMT and iPS-EMT upregulated both cardiac and skeletal muscle-specific genes and expressed Nkx2.5 and Myo-D proteins. MDSC-EMT displayed intracellular calcium ion transients and responses to isoproterenol. Contractile force measurements of MDSC-EMT demonstrated functional properties of immature cardiac and skeletal muscle in both tissues. Results suggest that the EMT from MDSCs mimics developing cardiac and skeletal muscle and can serve as a useful in vitro functioning striated muscle model for investigation of stem cell differentiation and therapeutic options of MDSCs for cardiac repair.
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Powers, Scott K. "Exercise: Teaching myocytes new tricks." Journal of Applied Physiology 123, no. 2 (2017): 460–72. http://dx.doi.org/10.1152/japplphysiol.00418.2017.

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Endurance exercise training promotes numerous cellular adaptations in both cardiac myocytes and skeletal muscle fibers. For example, exercise training fosters changes in mitochondrial function due to increased mitochondrial protein expression and accelerated mitochondrial turnover. Additionally, endurance exercise training alters the abundance of numerous cytosolic and mitochondrial proteins in both cardiac and skeletal muscle myocytes, resulting in a protective phenotype in the active fibers; this exercise-induced protection of cardiac and skeletal muscle fibers is often referred to as “exercise preconditioning.” As few as 3–5 consecutive days of endurance exercise training result in a preconditioned cardiac phenotype that is sheltered against ischemia-reperfusion-induced injury. Similarly, endurance exercise training results in preconditioned skeletal muscle fibers that are resistant to a variety of stresses (e.g., heat stress, exercise-induced oxidative stress, and inactivity-induced atrophy). Many studies have probed the mechanisms responsible for exercise-induced preconditioning of cardiac and skeletal muscle fibers; these studies are important, because they provide an improved understanding of the biochemical mechanisms responsible for exercise-induced preconditioning, which has the potential to lead to innovative pharmacological therapies aimed at minimizing stress-induced injury to cardiac and skeletal muscle. This review summarizes the development of exercise-induced protection of cardiac myocytes and skeletal muscle fibers and highlights the putative mechanisms responsible for exercise-induced protection in the heart and skeletal muscles.
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Dissertations / Theses on the topic "Skeletal and cardiac muscle"

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Walsh, Garrett Lyndon. "Skeletal muscle powered cardiac assist." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=63879.

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Kochamba, Gary. "Skeletal muscle powered cardiac assist." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61746.

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Lorusso, Roberto. "Cardiac reinforcement and assistance by electrically stimulated skeletal muscle." [Maastricht] : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1998. http://arno.unimaas.nl/show.cgi?fid=8398.

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Arnold, Michael Kevin. "Expression of calpastatin in porcine cardiac and skeletal muscle." Thesis, University of Nottingham, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294812.

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Ellison, Georgina May. "Myocyte death and regeneration in cardiac and skeletal muscle." Thesis, Liverpool John Moores University, 2004. http://researchonline.ljmu.ac.uk/5638/.

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Boraso, Antonella. "Pathophysiological aspects of the sheep cardiac sarcoplasmic reticulum calcium release channel." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265550.

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Burniston, Jatin George. "Clenbuterol-induced growth and damage of cardiac and skeletal muscle." Thesis, Liverpool John Moores University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400532.

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Brien, Patrick. "Postnatal regulation of proliferative capacity in skeletal and cardiac muscle." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708699.

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Kanaan, Georges. "Mitochondrial Dysfunction: From Mouse Myotubes to Human Cardiomyocytes." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37582.

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Mitochondrial dysfunction is a common feature in a wide range of disorders and diseases from obesity, diabetes, cancer to cardiovascular diseases. The overall goal of my doctoral research has been to investigate mitochondrial metabolic dysfunction in skeletal and cardiac muscles in the context of chronic disease development. Perinatal nutrition is well known to affect risk for insulin resistance, obesity, and cardiovascular disease during adulthood. The underlying mechanisms however, are poorly understood. Previous research from our lab showed that the in utero maternal undernutrition mouse model is one in which skeletal and cardiac muscle physiology and metabolism is impaired. Here we used this model to study the impact of in utero undernutrition on offspring skeletal primary muscle cells and to determine if there is a cell autonomous phenotype. Metabolic analyses using extracellular flux technologies revealed a shift from oxidative to glycolytic metabolism in primary myotubes. Gene expression profiling identified significant changes in mRNA expression, including an upregulation of cell stress and OXPHOS genes and a downregulation of cell division genes. However, there were no changes in levels of marker proteins for mitochondrial oxidative phosphorylation (OXPHOS). Findings are consistent with the conclusion that susceptibility to metabolic disease in adulthood can be caused at least in part by muscle defects that are programmed in utero and mediated by impaired mitochondrial function. In my second project, the effects of the absence of glutaredoxin-2 (Grx2) on redox homeostasis and on mitochondrial dynamics and energetics in cardiac muscle from mice were investigated. Previous work in our lab established that Grx2-deficient mice exhibit fibrotic cardiac hypertrophy, and hypertension, and that complex I of OXPHOS is defective in isolated mitochondria. Here we studied the role of Grx2 in the control of mitochondrial structure and function in intact cells and tissue, as well as the role of GRX2 in human heart disease. We demonstrated that the absence of Grx2 impacts mitochondrial fusion, ultrastructure and energetics in mouse primary cardiomyocytes and cardiac tissue and that provision of the glutathione precursor, N-acetylcysteine (NAC) did not restore glutathione redox or prevent impairments. Furthermore we used data from the human Genotype-Tissue Expression consortium to show that low GRX2 expression is associated with increased fibrosis, hypertrophy, and infarct in the left ventricle. Altogether, our results indicate that GRX2 plays a major role in cardiac mitochondrial structure and function, and protects against left ventricle pathologies in humans. In my third project, we collaborated with cardiac surgeon, Dr. Calum Redpath, of the Ottawa Heart Institute to study atrial mitochondrial metabolism in atrial fibrillation patients with and without type 2 diabetes (T2DM). T2DM is a major risk factor for atrial fibrillation, but the causes are poorly understood. Atrial appendages from coronary artery bypass graft surgery were collected and analyzed. We showed an impaired complex I respiration in diabetic patients with atrial fibrillation compared to diabetic patients without atrial fibrillation. In addition, and for the first time in atrial fibrillation patients, mitochondrial supercomplexes were studied; results showed no differences in the assembly of the “traditional” complexes but a decrease in the formation of “high oligomeric” complexes. A strong trend for increased protein oxidation was also observed. There were no changes in markers for OXPHOS protein levels. Overall findings reveal novel aspects of mitochondrial dysfunction in atrial fibrillation and diabetes in humans. Overall, our results reveal that in utero undernutrition affects the programming of skeletal muscle primary cells, thereby increasing susceptibility to metabolic diseases. In addition, we show that GRX2 impacts cardiac mitochondrial dynamics and energetics in both mice and humans. Finally, we show impaired mitochondrial function and supercomplex assembly in humans with atrial fibrillation and T2DM. Ultimately, understanding the mechanisms causing mitochondrial dysfunction in muscle tissues during chronic disease development will increase our capacity to identify effective prevention and treatment strategies.
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Duffy, Rebecca Marie. "Engineering Contractile 2D and 3D Human Skeletal and Cardiac Muscle Microtissues." Research Showcase @ CMU, 2016. http://repository.cmu.edu/dissertations/689.

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Skeletal and cardiac muscles are crucial biological actuators with limited capacity to repair themselves after significant trauma or disease states. Engineering these complex tissues using human derived cells has potential applications to serve as more physiologically relevant and economical test beds for regenerative medicine therapies compared to animal models and costly human trials. However, before we can engineer these tissues, we must first gain a better understanding of how the structure and composition of the extracellular matrix (ECM) influences differentiation and maturation into contractile muscle in vitro. To do this, we used traditional microcontact printing techniques to determine how ECM composition and line geometry influenced differentiating human skeletal muscle in 2D, and we incorporated these differentiating human myotubes into a muscular thin film (MTF) assay previously developed to measure 2D cardiomyocyte (CM) contractility. We also engineered contractile 3D cardiac microtissues with integrated force indicators (MIFIs) by seeding embryonic stem cell derived CMs and cardiac fibroblasts in biologically derived ECM hydrogels. From the 2D work, we found that human skeletal muscle derived cells had significantly higher myotube formation on laminin (LAM) lines, and C2C12 mouse myoblasts required more specific LAM line geometries than differentiating human skeletal muscle myoblasts to form uniaxially aligned myotubes. Additionally, we found that LAM with trace amounts of perlecan significantly increased human myotube formation compared to more purified LAM solutions. We also determined that 2D human skeletal muscle was limited to 1 week of differentiation before differentiating myoblasts delaminated from patterned polydimethylsiloxane. For the 3D engineered muscle constructs, we found that cardiac MIFIs could be maintained in culture for at least 2 weeks, exerted twitch forces ~1 - 7 μN and responded as expected to excitatory pharmacological stimuli. We developed the 3D MIFI assay using CMs with the intention of applying this platform to patient specific CMs from induced pluripotent stem cells as well as to differentiating skeletal muscle. The findings we have made by engineering contractile 2D human skeletal muscle and 3D human cardiac microtissues have future applications as patient specific regenerative therapy models, test beds for pharmaceutical therapies, building blocks for engineering functional muscle replacements, and as soft robotics actuators.
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Books on the topic "Skeletal and cardiac muscle"

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Heap, Sarah Heap. Microcirculation and performance in damaged skeletal and cardiac muscle. University of Birmingham, 1995.

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Bianchi, C. Paul, George B. Frank, and H. E. D. J. ter Keurs. Excitation-contraction coupling in skeletal, cardiac, and smooth muscle. Springer, 1992.

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Frank, George B., C. Paul Bianchi, and Henk E. D. J. ter Keurs, eds. Excitation-Contraction Coupling in Skeletal, Cardiac, and Smooth Muscle. Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3362-7.

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Blanck, Thomas J. J., and David M. Wheeler, eds. Mechanisms of Anesthetic Action in Skeletal, Cardiac, and Smooth Muscle. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5979-1.

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Schmalbruch, Henning. Skeletal muscle. Springer-Verlag, 1985.

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Schmalbruch, Henning. Skeletal Muscle. Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82551-4.

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McIntosh, Andrew. Different patterns of protein synthetic changes in skeletal,cardiac and smooth muscles of the rat in response to acute ethanol administered intraperitoneally and itragastrically. [University of Surrey], 1995.

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Canale, Enrico D., Gordon R. Campbell, Joseph J. Smolich, and Julie H. Campbell. Cardiac Muscle. Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-50115-9.

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Ryall, James G., ed. Skeletal Muscle Development. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7283-8.

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1957-, Prilutsky Boris I., ed. Biomechanics of skeletal muscle. Human Kinetics, 2012.

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Book chapters on the topic "Skeletal and cardiac muscle"

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Fietsam, Robert, and Larry W. Stephenson. "Myocardial Augmentation Using Skeletal Muscle." In Cardiac Surgery. Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3418-1_2.

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Hogan, Perry M., and Stephen R. Besch. "Vertebrate Skeletal and Cardiac Muscle." In Advances in Comparative and Environmental Physiology. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77115-6_4.

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Lund, Niels. "Skeletal and Cardiac Muscle Oxygenation." In Advances in Experimental Medicine and Biology. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-3291-6_3.

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Brown, Margaret D., and Olga Hudlická. "Angiogenesis in Skeletal and Cardiac Muscle." In The New Angiotherapy. Humana Press, 2002. http://dx.doi.org/10.1007/978-1-59259-126-8_14.

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Gibbs, C. L., and C. J. Barclay. "Efficiency of Skeletal and Cardiac Muscle." In Advances in Experimental Medicine and Biology. Springer US, 1998. http://dx.doi.org/10.1007/978-1-4684-6039-1_58.

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Kagan, V. E., V. B. Ritov, N. V. Gorbunov, E. Menshikova, and G. Salama. "Oxidative stress and Ca2+ transport in skeletal and cardiac sarcoplasmic reticulum." In Oxidative Stress in Skeletal Muscle. Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8958-2_11.

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Saks, Valdur A., A. V. Kuznetsov, Z. A. Huchua, and V. V. Kupriyanov. "Compartmentation of Adenine Nucleotides and Phosphocreatine Shuttle in Cardiac Cells: Some New Evidence." In Myocardial and Skeletal Muscle Bioenergetics. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5107-8_8.

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Lu, H., R. L. Hammond, G. A. Thomas, and L. W. Stephenson. "Skeletal Muscle Ventricles for Biologic Cardiac Assistance." In Assisted Circulation 4. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79340-0_19.

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Gordon, A. M., A. J. Rivera, C.-K. Wang, and M. Regnier. "Cooperative Activation of Skeletal and Cardiac Muscle." In Advances in Experimental Medicine and Biology. Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9029-7_34.

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Yamada, Hiroshi, and Eiichi Tanaka. "Active Stress Models of Cardiac Muscle, Smooth Muscle and Skeletal Muscle." In Human Biomechanics and Injury Prevention. Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-66967-8_21.

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Conference papers on the topic "Skeletal and cardiac muscle"

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Jarvis, J. C. "Electrical stimulation of skeletal muscle for cardiac assistance." In IEE Colloquium on Cardiac Pacing and Electrical Stimulation of the Heart. IEE, 1996. http://dx.doi.org/10.1049/ic:19960978.

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Urowitz, Murray. "02 Hydroxychloroquine myopathy: cardiac and skeletal muscle toxicity." In 10th Annual Meeting of the Lupus Academy. Lupus Foundation of America, 2021. http://dx.doi.org/10.1136/lupus-2021-la.2.

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Cassino, Theresa R., Masaho Okada, Lauren Drowley, Johnny Huard, and Philip R. LeDuc. "Mechanical Stimulation Improves Muscle-Derived Stem Cell Transplantation for Cardiac Repair." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192941.

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Muscle-derived stem cells (MDSCs) have been successfully transplanted into both skeletal (1) and cardiac muscle (2) of dystrophin-deficient (mdx) mice, and show potential for improving cardiac and skeletal dysfunction in diseases like Duchenne muscular dystrophy (DMD). Our previous study explored the regeneration of dystrophin-expressing myocytes following MDSC transplantation into environments with distinct blood flow and chemical/mechanical stimulation attributes. After MDSC transplantation within left ventricular myocardium and gastrocnemius (GN) muscles of the same mdx mice, significantly more dystrophin-positive fibers were found within the myocardium than in the GN. We hypothesized that the differences in mechanical loading of the two environments influenced the transplantation and explored whether using MDSCs exposed to mechanical stimulation prior to transplantation could improve transplantation. Our study shows increased engraftment into the heart and GN muscle for cells pretreated with mechanical stretch for 24 hours. This increase was significant for transplantation into the heart. These studies have implications in a variety of applications including mechanotransduction, stem cell biology, and Duchenne muscular dystrophy.
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Heyne, E., M. Schwarzer, S. Zeeb, L. G. Koch, L. Britton, and T. Doenst. "Differential Effects of Exercise on Interfibrillar and Subsarcolemmal Skeletal Muscle Mitochondria." In 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678818.

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Cassino, Theresa R., Masaho Okada, Lauren M. Drowley, Joseph Feduska, Johnny Huard, and Philip R. LeDuc. "Using Mechanical Environment to Enhance Stem Cell Transplantation in Muscle Regeneration." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176545.

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Muscle-derived stem cell (MDSC) transplantation has shown potential as a therapy for cardiac and skeletal muscle dysfunction in diseases such as Duchenne muscular dystrophy (DMD). In this study we explore mechanical environment and its effects on MDSCs engraftment into cardiac and skeletal muscle in mdx mice and neoangiogenesis within the engraftment area. We first looked at transplantation of the same number of MDSCs into the heart and gastrocnemius (GN) muscle of dystrophic mice and the resulting dystrophin expression. We then explored neoangiogenesis within the engraftments through quantification of CD31 positive microvessels. This study is important to aid in determining the in vivo environmental factors leading to large graft size which may aid in determining optimum transplantation conditions for muscle repair.
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Lopata, R. G. P., I. H. Gerrits, J. M. Thijssen, et al. "2H-1 In Vivo 3D Cardiac and Skeletal Muscle Strain Estimation." In 2006 IEEE Ultrasonics Symposium. IEEE, 2006. http://dx.doi.org/10.1109/ultsym.2006.198.

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Salmons and Jarvis. "Skeletal Muscle As An Adaptive Contractile Biomaterial For Cardiac Assistance: Fundamental Considerations." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.593795.

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Salmons, Stanley, and Jonathan C. Jarvis. "Skeletal muscle as an adaptive contractile biomaterial for cardiac assistance: Fundamental considerations." In 1992 14th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.5761695.

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Schwarzer, M., S. Zeeb, E. Heyne, L. G. Koch, L. Britton, and T. Doenst. "Differences in Skeletal and Heart Muscle Mitochondrial Function in Response to Intrinsic and Acquired Exercise Capacity." In 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678822.

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Golubev, A. I., M. A. Kupriyanova, M. M. Salnikova, and V. R. Saitov. "CYTOMORPHOLOGICAL CHANGES IN THE CARDIAC AND SKELETAL MUSCLE TISSUE OF RABBITS IN LEAD INTOXICATIONS." In STATE AND DEVELOPMENT PROSPECTS OF AGRIBUSINESS Volume 2. DSTU-Print, 2020. http://dx.doi.org/10.23947/interagro.2020.2.475-478.

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The pollution and accumulation of lead and its compounds in the natural environment every year poses an increasing threat to human health and natural ecosystems. This problem is the most serious in megacities. The established criteria and the results of practical studies indicate lead as one of the most dangerous ecotoxicants. In the present work, the effect of lead acetate on the body of productive animals was analyzed, and cytomorphological and ultrastructural changes in the heart and striated (skeletal) muscle tissue were revealed. Visual disorders are confirmed by morphometric analysis.
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Reports on the topic "Skeletal and cardiac muscle"

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Owen, Laura. Calcium and Redox Control of the Calcium Release Mechanism of Skeletal and Cardiac Muscle Sarcoplasmic Reticulum. Portland State University Library, 2000. http://dx.doi.org/10.15760/etd.430.

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Walters, Thomas. Engineered Skeletal Muscle for Craniofacial Reconstruction. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada601864.

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Buck, Edmond. Mechanism of Calcium Release from Skeletal Muscle Sarcoplasmic Reticulum. Portland State University Library, 2000. http://dx.doi.org/10.15760/etd.1306.

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Koh, Timothy J. Enhancement of Skeletal Muscle Repair by the Urokinase-Type Plasminogen Activator System. Defense Technical Information Center, 2006. http://dx.doi.org/10.21236/ada448526.

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Xiong, Hui. Modification of the CA²⁺ Release Channel from Sarcoplasmic Reticulum of Skeletal Muscle. Portland State University Library, 2000. http://dx.doi.org/10.15760/etd.1303.

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Wagner, Mark. The physiology and biochemistry of isolated skeletal muscle mitochondria : a comparative study. Portland State University Library, 2000. http://dx.doi.org/10.15760/etd.5842.

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Wilmore, Douglas W. A Program for the Study of Skeletal Muscle Catabolism Following Physical Trauma. Defense Technical Information Center, 1989. http://dx.doi.org/10.21236/ada216569.

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Stuart, Janice. Chemical Modification of Skeletal Muscle Sarcoplasmic Reticulum Vesicles: A Study of Calcium Permeability. Portland State University Library, 2000. http://dx.doi.org/10.15760/etd.1388.

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Goerke, Ute. Proteolytic modification of the Ca²-release mechanism of sarcoplasmic reticulum in skeletal muscle. Portland State University Library, 2000. http://dx.doi.org/10.15760/etd.6101.

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Dornan, Thomas. Antioxidant Anthocyanidins and Calcium Transport Modulation of the Ryanodine Receptor of Skeletal Muscle (RyR1). Portland State University Library, 2000. http://dx.doi.org/10.15760/etd.319.

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