Relevant bibliographies by topics / Skeletal Muscles

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

Academic literature on the topic 'Skeletal Muscles'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "Skeletal Muscles"

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Lieber, Richard L., and Samuel R. Ward. "Skeletal muscle design to meet functional demands." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1570 (May 27, 2011): 1466–76. http://dx.doi.org/10.1098/rstb.2010.0316.

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Skeletal muscles are length- and velocity-sensitive force producers, constructed of a vast array of sarcomeres. Muscles come in a variety of sizes and shapes to accomplish a wide variety of tasks. How does muscle design match task performance? In this review, we outline muscle's basic properties and strategies that are used to produce movement. Several examples are provided, primarily for human muscles, in which skeletal muscle architecture and moment arms are tailored to a particular performance requirement. In addition, the concept that muscles may have a preferred sarcomere length operating range is also introduced. Taken together, the case is made that muscles can be fine-tuned to perform specific tasks that require actuators with a wide range of properties.
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Kholodnyi, R. D. "MODELING THE SKELETAL MUSCLE INJURY IN RATS." International Journal of Veterinary Medicine, no. 3 (October 18, 2022): 253–57. http://dx.doi.org/10.52419/issn2072-2419.2022.3.253.

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Muscles are the most important executive organs - effectors. Both according to morphological and functional characteristics, muscles are divided into two types - striated and smooth. Striated muscles, in turn, are usually divided into skeletal and cardiac. Striated muscles form the motor apparatus of the skeleton, oculomotor, chewing and other motor systems in animals. The striated muscles, with the exception of the heart muscle, are completely controlled by the central nervous system, they are devoid of automatism.The problem of damage to skeletal muscles is very relevant and widespread. These injuries disrupt the musculoskeletal function of animals, up to its complete loss. To search for methods for restoring the structure and function of muscles, experiments are being carried out on laboratory animals. This article is devoted to the selection of the optimal model of skeletal muscle injury, performed on laboratory rats. The study was conducted on Wistar rats. The choice of the muscle on which the models will be worked out, as well as the surgical access to it, is substantiated. Three options for inflicting damage to muscle tissue (cut wounds directed parallel to muscle fibers; cut wounds directed across muscle fibers; crushed wounds of muscle tissue) and the timing of healing of these injuries are proposed. The result of the study showed that the gastrocnemius muscle is the most suitable for modeling damage to muscle tissue in rats, and a crushed wound has the longest healing time.
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Testa, Marco, Bianca Rocca, Lucia Spath, Franco O. Ranelletti, Giovanna Petrucci, Giovanni Ciabattoni, Fabio Naro, Stefano Schiaffino, Massimo Volpe, and Carlo Reggiani. "Expression and activity of cyclooxygenase isoforms in skeletal muscles and myocardium of humans and rodents." Journal of Applied Physiology 103, no. 4 (October 2007): 1412–18. http://dx.doi.org/10.1152/japplphysiol.00288.2007.

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Conflicting data have been reported on cyclooxygenase (COX)-1 and COX-2 expression and activity in striated muscles, including skeletal muscles and myocardium, in particular it is still unclear whether muscle cells are able to produce prostaglandins (PGs). We characterized the expression and enzymatic activity of COX-1 and COX-2 in the skeletal muscles and in the myocardium of mice, rats and humans. By RT-PCR, COX-1 and COX-2 mRNAs were observed in homogenates of mouse and rat hearts, and in different types of skeletal muscles from all different species. By Western blotting, COX-1 and -2 proteins were detected in skeletal muscles and hearts from rodents, as well as in skeletal muscles from humans. Immunoperoxidase stains showed that COX-1 and -2 were diffusely expressed in the myocytes of different muscles and in the myocardiocytes from all different species. In the presence of arachidonic acid, which is the COX enzymatic substrate, isolated skeletal muscle and heart samples from rodents released predominantly PGE2. The biosynthesis of PGE2 was reduced between 50 and 80% ( P < 0.05 vs. vehicle) in the presence of either COX-1- or COX-2-selective blockers, demonstrating that both isoforms are enzymatically active. Exogenous PGE2 added to isolated skeletal muscle preparations from rodents did not affect contraction, whereas it significantly fastened relaxation of a slow type muscle, such as soleus. In conclusion, COX-1 and COX-2 are expressed and enzymatically active in myocytes of skeletal muscles and hearts of rodents and humans. PGE2 appears to be the main product of COX activity in striated muscles.
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Heo, Jun-Won, Su-Zi Yoo, Mi-Hyun No, Dong-Ho Park, Ju-Hee Kang, Tae-Woon Kim, Chang-Ju Kim, et al. "Exercise Training Attenuates Obesity-Induced Skeletal Muscle Remodeling and Mitochondria-Mediated Apoptosis in the Skeletal Muscle." International Journal of Environmental Research and Public Health 15, no. 10 (October 19, 2018): 2301. http://dx.doi.org/10.3390/ijerph15102301.

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Obesity is characterized by the induction of skeletal muscle remodeling and mitochondria-mediated apoptosis. Exercise has been reported as a positive regulator of skeletal muscle remodeling and apoptosis. However, the effects of exercise on skeletal muscle remodeling and mitochondria-mediated apoptosis in obese skeletal muscles have not been clearly elucidated. Four-week-old C57BL/6 mice were randomly assigned into four groups: control (CON), control plus exercise (CON + EX), high-fat diet (HFD), and HFD plus exercise groups (HFD + EX). After obesity was induced by 20 weeks of 60% HFD feeding, treadmill exercise was performed for 12 weeks. Exercise ameliorated the obesity-induced increase in extramyocyte space and a decrease in the cross-sectional area of the skeletal muscle. In addition, it protected against increases in mitochondria-mediated apoptosis in obese skeletal muscles. These results suggest that exercise as a protective intervention plays an important role in regulating skeletal muscle structure and apoptosis in obese skeletal muscles.
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J Rosochacki, S., T. Sakowski, J. Połoszynowicz, E. Juszczuk-Kubiak, A. Kowalik-Krupa, and J. Oprządek. "Lysosomal proteolysis in skeletal muscles of bulls." Czech Journal of Animal Science 49, No. 8 (December 13, 2011): 340–48. http://dx.doi.org/10.17221/4318-cjas.

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The relationship between lysosomal proteolytic enzyme activities involved in skeletal muscle proteolysis of the longissimus lumborum et thoracis muscle (MLLT) of bulls was described. Samples from the same region were obtained post mortem from 7 Piemontese (P) and 54 Black-and-White bulls (B-W) about 18 months old fed ad libitum. The activity of cathepsin D was determined as pepstatin (cathepsin D inhibitor) sensitive activity (PSCatD) towards 1% haemoglobin. Pepstatin-insensitive acid (PIA) and leupeptin-insensitive (thiol proteinase inhibitor) acid (LIA) autolytic activities were measured in the presence of 1 mM Mg<sup>++</sup>. MLLT was also analysed for RNA, DNA and protein content. The data were processed by analysis of variance and differences between sires were tested by the contrast procedure of general linear model. In the examined muscle RNA decreased by 16% in B-W compared to P, CPS by about 14% and FCS by about 39%. DNA content was higher by 64.5% in B-W compared to P bulls (P&nbsp;&le; 0.01). Some differences were found between P bulls and B-W groups of sires in the percentage of proteins (P &le; 0.01), CatD and PSCatD (P &le; 0.01), but the most pronounced differences were determined in PIA and LIA (P &le; 0.01), and in the percentage of inhibition by pepstatin and leupeptin (P &le; 0.01) in AAA. In the Black-and-White group of sires the percentage of protein and percentage of inhibition by pepstatin and leupeptin in AAA were lowered by about 10, 17 and 22%, but PSCatD, PIA and LIA were higher by about 23.7, 41 and 57.7%, respectively, compared to Piemontese bulls. The level of aspartic and thiol proteinases was lower in the muscles of B-W compared to Piemontese. The activity was much higher in B-W compared to P. These results indicate the faster turnover of proteins in the groups after Black-and-White sires and higher anabolic increase in degradation in Piemontese bulls. &nbsp; &nbsp;
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Kostrominova, Tatiana Y., Douglas E. Dow, Robert G. Dennis, Richard A. Miller, and John A. Faulkner. "Comparison of gene expression of 2-mo denervated, 2-mo stimulated-denervated, and control rat skeletal muscles." Physiological Genomics 22, no. 2 (July 14, 2005): 227–43. http://dx.doi.org/10.1152/physiolgenomics.00210.2004.

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Loss of innervation in skeletal muscles leads to degeneration, atrophy, and loss of force. These dramatic changes are reflected in modifications of the mRNA expression of a large number of genes. Our goal was to clarify the broad spectrum of molecular events associated with long-term denervation of skeletal muscles. A microarray study compared gene expression profiles of 2-mo denervated and control extensor digitorum longus (EDL) muscles from 6-mo-old rats. The study identified 121 genes with increased and 7 genes with decreased mRNA expression. The expression of 107 of these genes had not been identified previously as changed after denervation. Many of the genes identified were genes that are highly expressed in skeletal muscles during embryonic development, downregulated in adults, and upregulated after denervation of muscle fibers. Electrical stimulation of denervated muscles preserved muscle mass and maximal force at levels similar to those in the control muscles. To understand the processes underlying the effect of electrical stimulation on denervated skeletal muscles, mRNA and protein expression of a number of genes, identified by the microarray study, was compared. The hypothesis was that loss of nerve action potentials and muscle contractions after denervation play the major roles in upregulation of gene expression in skeletal muscles. With electrical stimulation of denervated muscles, the expression levels for these genes were significantly downregulated, consistent with the hypothesis that loss of action potentials and/or contractions contribute to the alterations in gene expression in denervated skeletal muscles.
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Park, Song-Young, Jayson R. Gifford, Robert H. I. Andtbacka, Joel D. Trinity, John R. Hyngstrom, Ryan S. Garten, Nikolaos A. Diakos, 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 (August 1, 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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Eržen, Ida. "PLASTICITY OF SKELETAL MUSCLE STUDIED BY STEREOLOGY." Image Analysis & Stereology 23, no. 3 (May 3, 2011): 143. http://dx.doi.org/10.5566/ias.v23.p143-152.

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The present contribution provides an overview of stereological methods applied in the skeletal muscle research at the Institute of Anatomy of the Medical Faculty in Ljubljana. Interested in skeletal muscle plasticity we studied three different topics: (i) expression of myosin heavy chain isoforms in slow and fast muscles under experimental conditions, (ii) frequency of satellite cells in young and old human and rat muscles and (iii) capillary supply of rat fast and slow muscles. We analysed the expression of myosin heavy chain isoforms within slow rat soleus and fast extensor digitorum longus muscles after (i) homotopic and heterotopic transplantation of both muscles, (ii) low frequency electrical stimulation of the fast muscle and (iii) transposition of the fast nerve to the slow muscle. The models applied were able to turn the fast muscle into a completely slow muscle, but not vice versa. One of the indicators for the regenerative potential of skeletal muscles is its satellite cell pool. The estimated parameters, number of satellite cells per unit fibre length, corrected to the reference sarcomere length (Nsc/Lfib) and number of satellite cells per number of nuclei (myonuclei and satellite cell nuclei) (Nsc/Nnucl) indicated that the frequency of M-cadherin stained satellite cells declines in healthy old human and rat muscles compared to young muscles. To access differences in capillary densities among slow and fast muscles and slow and fast muscle fibres, we have introduced Slicer and Fakir methods, and tested them on predominantly slow and fast rat muscles. Discussing three different topics that require different approach, the present paper reflects the three decades of the development of stereological methods: 2D analysis by simple point counting in the 70's, the disector in the 80's and virtual spatial probes in the 90's. In all methods the interactive computer assisted approach was utilised.
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Gomez-Cabrera, M. C., G. L. Close, A. Kayani, A. McArdle, J. Viña, and M. J. Jackson. "Effect of xanthine oxidase-generated extracellular superoxide on skeletal muscle force generation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 1 (January 2010): R2—R8. http://dx.doi.org/10.1152/ajpregu.00142.2009.

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Skeletal muscle contractions increase superoxide anion in skeletal muscle extracellular space. We tested the hypotheses that 1) after an isometric contraction protocol, xanthine oxidase (XO) activity is a source of superoxide anion in the extracellular space of skeletal muscle and 2) the increase in XO-derived extracellular superoxide anion during contractions affects skeletal muscle contractile function. Superoxide anion was monitored in the extracellular space of mouse gastrocnemius muscles by following the reduction of cytochrome c in muscle microdialysates. A 15-min protocol of nondamaging isometric contractions increased the reduction of cytochrome c in microdialysates, indicating an increase in superoxide anion. Mice treated with the XO inhibitor oxypurinol showed a smaller increase in superoxide anions in muscle microdialysates following contractions than in microdialysates from muscles of vehicle-treated mice. Intact extensor digitorum longus (EDL) and soleus muscles from mice were also incubated in vitro with oxypurinol or polyethylene glycol-tagged Cu,Zn-SOD. Oxypurinol decreased the maximum tetanic force produced by EDL and soleus muscles, and polyethylene glycol-tagged Cu,Zn-SOD decreased the maximum force production by the EDL muscles. Neither agent influenced the rate of decline in force production when EDL or soleus muscles were repeatedly electrically stimulated using a 5-min fatiguing protocol (stimulation at 40 Hz for 0.1 s every 5 s). Thus these studies indicate that XO activity contributes to the increased superoxide anion detected within the extracellular space of skeletal muscles during nondamaging contractile activity and that XO-derived superoxide anion or derivatives of this radical have a positive effect on muscle force generation during isometric contractions of mouse skeletal muscles.
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Wu, G. Y., and J. R. Thompson. "Is methionine transaminated in skeletal muscle?" Biochemical Journal 257, no. 1 (January 1, 1989): 281–84. http://dx.doi.org/10.1042/bj2570281.

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Methionine transamination is extensive in rat and chick skeletal-muscle homogenates, but is barely detectable in intact rat, but not chick, skeletal muscles. Branched-chain amino acids essentially block methionine transamination in intact muscles and homogenates from both species. The physiological significance of methionine transamination in skeletal muscle is questioned.
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Dissertations / Theses on the topic "Skeletal Muscles"

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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 musculaire
Musculoskeletal 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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Books on the topic "Skeletal Muscles"

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L, Mastaglia Frank, and Walton John Nicholas, eds. Skeletal muscle pathology. 2nd ed. Edinburgh: Churchill Livingstone, 1992.

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

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A, Stone Judith, ed. Atlas of skeletal muscles. 3rd ed. Boston: McGraw-Hill, 2000.

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Stone, Robert J. Atlas of skeletal muscles. 6th ed. Boston: McGraw-Hill Higher Education, 2009.

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Stone, Robert J. Atlas of skeletal muscles. 6th ed. Boston: McGraw-Hill Higher Education, 2009.

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A, Stone Judith, ed. Atlas of skeletal muscles. 6th ed. Boston: McGraw-Hill Higher Education, 2009.

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Stone, Robert J. Atlas of skeletal muscles. 2nd ed. Dubuque, IA: Wm. C. Brown Publishers, 1997.

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A, Stone Judith, ed. Atlas of skeletal muscles. 7th ed. New York: McGraw-Hill, 2011.

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

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1955-, Herzog W., ed. Skeletal muscle mechanics: From mechanisms to function. Chichester, UK: John Wiley, 2000.

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Book chapters on the topic "Skeletal Muscles"

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Schmalbruch, H. "Muscle Fibre Types in Mammalian Muscles." In Skeletal Muscle, 159–204. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82551-4_4.

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Ritchison, Gary. "Skeleton and Skeletal Muscles." In In a Class of Their Own, 155–317. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-14852-1_2.

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Saghiv, Moran S., and Michael S. Sagiv. "Skeletal Muscles." In Basic Exercise Physiology, 407–36. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-48806-2_8.

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Schmalbruch, H. "Non-Skeletal Muscles." In Skeletal Muscle, 217–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82551-4_6.

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Scadding, J. G., and D. N. Mitchell. "Bones, Joints and Skeletal Muscles." In Sarcoidosis, 227–51. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4899-2971-6_9.

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Stager, Joel M. "Peripheral Adaptations: The Skeletal Muscles." In Handbook of Sports Medicine and Science: Swimming, 35–50. Oxford, UK: Blackwell Science Ltd, 2008. http://dx.doi.org/10.1002/9780470698761.ch3.

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Lipková, Janka. "Mitochondrial Bioenergetics of Skeletal Muscles." In Mitochondrial Medicine, 189–200. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6714-3_10.

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Kohli, Vinay Kumar, Chitra Kohli, and Akanksha Singh. "Peripheral Nerves and Skeletal Muscles." In Comprehensive Multiple-Choice Questions in Pathology, 169–74. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-08767-7_21.

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Subramani, V., V. Sahgal, S. Sahgal, and H. Kochar. "Distribution of muscle spindles in primate skeletal muscles." In The Muscle Spindle, 89–93. London: Palgrave Macmillan UK, 1985. http://dx.doi.org/10.1007/978-1-349-07695-6_12.

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Tanaka, Eiji, Kumiko Nagata, and Nobuhiko Kawai. "Application of LIPUS to Skeletal Muscles." In Therapeutic Ultrasound in Dentistry, 27–34. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-66323-4_4.

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Conference papers on the topic "Skeletal Muscles"

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Odegard, G. M., T. L. Haut Donahue, D. A. Morrow, and K. R. Kaufman. "Constitutive Modeling of Skeletal Muscle Tissue." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-175848.

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The main functions of the human musculoskeletal system are to sustain loads and provide mobility. Bones and joints themselves cannot produce movement; skeletal muscles provide the ability to move. Knowledge of muscle forces during given activities can provide insight into muscle mechanics, muscle physiology, musculoskeletal mechanics, neurophysiology, and motor control. However, clinical examinations or instrumented strength testing only provides information regarding muscle groups. Musculoskeletal models are typically needed to calculate individual muscle forces.
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Begun, Petr I., Konstantin N. Bolsunov, Elena A. Lebedeva, and Oksana V. Krivokhizhina. "Biomechanical modeling of skeletal muscles reconstruction." In 2016 XIX IEEE International Conference on Soft Computing and Measurements (SCM). IEEE, 2016. http://dx.doi.org/10.1109/scm.2016.7519695.

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Li, Linlin, and John Boss. "Skeletal Muscles Modeling for Isogeometric Analysis." In 2018 7th International Conference on Energy and Environmental Protection (ICEEP 2018). Paris, France: Atlantis Press, 2018. http://dx.doi.org/10.2991/iceep-18.2018.6.

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Novotny, John E., Brian A. Knarr, and Hehe Zhou. "Maximum Contractile Strain in the Biceps Brachii Is Bounded by Sarcomere Geometry." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192589.

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Skeletal muscles’ primary function is the application of force to its bony origins and insertions. There are various models of muscle function that generally assume a uniform behavior from origin to insertion during force generation even though the structure and activation is complex. Engineering strains within skeletal muscles, though, have been shown to be non-uniform [1]. We have developed methods to quantify Lagrangian finite strains using cine phase-contrast magnetic resonance imaging (CPCMRI) and post-processing algorithms [2] and have described them during cyclic motion in the supraspinatus and biceps brachii. Principal and maximum in-plane shear strains can be identified at the scale of millimeters throughout the contracting and elongating muscle.
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Al-Ibadi, Alaa, Samia Nefti-Meziani, and Steve Davis. "A circular pneumatic muscle actuator (CPMA) inspired by human skeletal muscles." In 2018 IEEE International Conference on Soft Robotics (RoboSoft). IEEE, 2018. http://dx.doi.org/10.1109/robosoft.2018.8404889.

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Ramirez, Angelica Maria, Begoña Calvo Calzada, and Jorge Grasa. "The Effect of the Fascia on the Stress Distribution in Skeletal Muscle." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19696.

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The human and vertebrate interaction with the environment is done primarily through the movement. This is possible due the skeletal muscle: anatomical structure able to contract voluntarily. The skeletal muscles are made up of contractile proteins which slide one over another allowing the muscle shortening and the body force generation. This protein structure of actin and myosin maintains its organization through the connective tissue that surrounds it (endomysium, perimysium and epimysium), creating arrays of myofibrils, fibre bundles, fascicles until conform the whole muscle. All this connective tissue extends to the ends of the muscle to form the tendon.
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Linder-Ganz, Eran, and Amit Gefen. "The Effects of Pressure and Shear on Capillary Closure in the Microstructure of Skeletal Muscles: Computational Studies." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176516.

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Deep tissue injury (DTI) is a serious and potentially deadly type of pressure ulcers, which initiate in deep muscle tissue under bony prominences of immobilized patients, and progress outwards towards the skin with no clear visual indications of the injury at the surface of the body. It had been suggested that DTI appear in muscle tissue first, due to the dense capillary vasculature in skeletal muscles which is susceptible to obstruction and occlusion by mechanical forces [1–3]. Though mechanical forces may cause capillaries to collapse and thus induce ischemic conditions in adjacent muscle cells [2], some investigators stipulated that ischemia alone cannot explain the etiology of DTI, and so, other mechanisms, particularly excessive cellular deformations must be involved [1]. We hypothesize that physiological levels of stresses and strains in muscle tissue under bony prominences — even when muscles are highly loaded as during sitting — do not cause complete closure of muscle capillaries, and therefore, do not cause an acute ischemia in muscles. If this is indeed the case, then ischemia cannot be the only factor contributing to DTI onset. In order to test our hypothesis, we developed a finite element (FE) model of the microstructure of skeletal muscle, at the level of muscle fascicles, and employed the model to determine the stress and strain levels required for causing partial and complete closure of capillaries.
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Ahmed, Amira, Huda Farah, Omnia Ahmed, Dina Elsayegh, Abdelrahman Elgamal, and Nasser Moustafa Rizk. "Profile Of Oxidative Stress Genes In Response To Obesity Treatment." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0150.

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Background: Oxidative stress (OS) is an imbalance between free radical production and the antioxidants defense in the body. Previous studies demonstrated the correlation of OS to the increased risk of developing metabolic disorders such as obesity. Sulforaphane (SFN), a bioactive compound, can protect against inflammation and OS, thus an effective anti-obesity supplement. Aim: This study explores the impact of SNF on OS in diet induced obese (DIO) mice via profiling of OS genes and pathways in skeletal muscles related to the anti-obesity effect. Methods: Wild-type CD1 male mice and the knockout of nuclear factor (erythroid-derived 2) like 2 (NrF2) mice were fed a high-fat diet (HFD) for 16 weeks; to induce obesity. Subsequently, each group was subdivided into two subgroups and received either Vehicle (25μl) or SFN (5 mg/kg BW) for four weeks. Body weight was measured daily, and a glucose tolerance test (GTT) was performed after 21 days of treatment. Afterward, mice were decapitated, blood and tissue samples were collected and snap-frozen immediately. Total RNA was extracted from Skeletal muscle and epididymal white adipose tissue (eWAT), leptin expression was measured in (eWAT), and 84 OS genes in skeletal muscle were examined using RT-PCR. Results: Significant reduction in body weight in SFN treated WT mice, while no change in KO mice. Plasma glucose, leptin, and leptin gene expression (eWAT) were significantly reduced in the WT-DIO SFN treated group, while no changes were detected in KO mice. SFN decreases OS damage in skeletal muscles, such as lipid peroxidation and production of reactive oxygen species (ROS). Conclusion: This study demonstrated that SFN had lowered body weight in WT-DIO mice by decreasing OS damage in skeletal muscles through the NrF2 pathway and can be a potential anti-obesity drug.
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Wagner, Hallie, Dawn Lowe, and Victor Barocas. "Reduced Compliance in Patellar Tendons From a Mouse Model of Muscular Dystrophy." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80762.

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Muscular dystrophies are degenerative diseases that affect primarily skeletal muscles. Most studies of muscular dystrophy focus on muscles, but tendons are an important part of the musculotendon complex that transmits forces from muscles to bones. As the disease progresses, tendon shortening occurs, and some patients require tendon release or cord lengthening surgery to increase tendon length [1]. Despite the prevalence of these surgeries, very little is known about the mechanical properties of tendons in muscular dystrophy patients, or how they change as the tendon remodels or compensate in response to muscle degeneration.
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Gijsbertse, Kaj, Andre M. Sprengers, Maartje M. Nillesen, Hendrik H. G. Hansen, Nico Verdonschot, and Chris L. de Korte. "Three-dimensional ultrasound strain imaging of skeletal muscles." In 2015 IEEE International Ultrasonics Symposium (IUS). IEEE, 2015. http://dx.doi.org/10.1109/ultsym.2015.0179.

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Reports on the topic "Skeletal Muscles"

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C. Uy, Genevieve, Raymond L. Rosales, and Satish Khadilkar. Myopathies in Clinical Care: A Focus on Treatable Causes. Progress in Neurobiology, February 2024. http://dx.doi.org/10.60124/j.pneuro.2024.10.01.

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Myopathies present a wide range of clinical symptoms that affect the skeletal muscles, including weakness, fatigue, and pain. While acquired myopathies receive significant attention due to the availability of treatment options, it is important to note that some inherited myopathies can also be effectively managed. These myopathies can be classified based on their underlying causes, such as infectious agents, autoimmune disorders leading to muscle inflammation, granulomatous inflammation, metabolic abnormalities within the muscle cells, skeletal muscle channel dysfunctions, prolonged ICU stay, and inherited conditions such as Duchenne muscular dystrophy. In this review, we initially present a clinical approach to neuromuscular diseases and subsequently place specific emphasis on myopathies, particularly to those that have treatment options available.
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Kanner, Joseph, Dennis Miller, Ido Bartov, John Kinsella, and Stella Harel. The Effect of Dietary Iron Level on Lipid Peroxidation of Muscle Food. United States Department of Agriculture, January 1995. http://dx.doi.org/10.32747/1995.7604282.bard.

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Biological oxidations are almost exclusively metal ion-promoted reactions and in ths respect iron, being the most abundant, is the commonly involved. The effect of dietary iron levels on pork, turkey and chick muscle lipid peroxidation and various other related compounds were evaluated. Crossbred feeder pigs were fed to market weight on corn-soy rations containing either 62, 131 or 209 ppm iron. After slaughter, the muscles were dissected, cooked and stored at 4°C. Heavily fortifying swine rations with iron (>200 ppm) increase nn-heme iron (NHI), thiobarbituric acid reactive substances (TBARS), and decrease a-tocopherol in cooked stored pork but did not increase warmed-over aroma (WOA). NHI and TBARS were higher in cooked pork from pigs fed high-iron diets. Liver iron correlated with muscle iron. TBARS were strongly related with WOA. The role of dietary vitamin E and ascorbic acid on Fe-induced in vivo lipid peroxidation in swine was also evaluated. Moderate elevation in iron stores had a marked effect on oxidative stress, especially as indicated by liver TBARS. Supplemental vitamin E, and to a lesser extent vitamin C, protect against this oxidative stress. Unsupplementation of Fe in the regular diet of turkeys did not affect body weight, blood hemoglobin level, or iron pool in the liver or muscle. The reason being that it contained "natural" ~120 mg Fe/kg feed, and this amount is high enough to keep constant the pool of iron in the body, liver or muscle tissues. Only Fe-supplementation with high amounts of Fe (500 ppm) significantly increased turkey blood hemoglobin and total iron in the liver, in 1 out of 3 experiments, but only slightly affects iron pool in the muscles. It seems that the liver accumulates very high concentations of iron and significantly regulates iron concentration in skeletal muscles. For this reason, it was very difficult to decrease muscle stability in turkeys through a diet containing high levels of Fe-supplementation. It was shown that the significant increase in the amount of iron (total and "free") in the muscle by injections with Fe-dextran accelerated its lipid peroxidation rate and decreased its a-tocopherol concentration. The level and metabolism of iron in the muscles affects the intensity of in vivo lipid peroxidation. This process was found to ifluence the turnover and accumulation of a-tocopherol in turkey and chick muscles. Treatments which could significantly decrease the amount and metabolism of iron pool in muscle tissues (or other organs) may affect the rate of lipid peroxidation and the turnover of a-tocopherol. Several defense enzymes were determined and found in the turkey muscle, such as superoxide dismutase, catalase, and glutathione peroxidase. Glutathione peroxidase was more active in muscles with a high trend of lipid peroxidation, lmore so in drumsticks than in breast muscles, or muscles with a low a-tocopherol content. The activity of glutathione peroxidase increased several fold in muscle stored at 4°C. Our work demonstrated that it will be much more practical to increase the stability of muscle tissues in swine, turkeys and chickens during storage and processing by increasing the amount of vitamin E in the diet than by withdrawing iron supplementation.
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Jalil, Yorschua, and Ruvistay Gutierrez. Myokines secretion and their role in critically ill patients. A scoping review protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2021. http://dx.doi.org/10.37766/inplasy2021.9.0048.

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Review question / Objective: 1-How and by which means stimulated muscle from critically ill patients can liberate myokines?, 2-Which are the main characteristics of the critically ill population studied and if some of these influenced myokine´s secretion?, 5-Can myokines exert local or distant effects in critically ill patients?, 5-Which are the potential effects of myokines in critically ill patients? Eligibility criteria: Participants and context: We will include primary studies (randomized or non-randomized trials, observational studies, case series or case report) that consider hospitalized critically ill adult patients (18 years or older) in risk for developing some degree of neuromuscular disorders such as ICU-AW, diaphragmatic dysfunction, or muscle weakness, therefore the specific setting will be critical care. Concept: This review will be focused on studies regarding the secretion or measure of myokines or similar (exerkines, cytokines or interleukin) by any mean of muscle activation or muscle contraction such as physical activity, exercise or NMES, among others. The latter strategies must be understood as any mean by which muscle, and there for myocytes, are stimulated as result of muscle contraction, regardless of the frequency, intensity, time of application and muscle to be stimulated (upper limb, lower limb, thoracic or abdominal muscles). We also will consider myokine´s effects, local or systemic, over different tissues in terms of their structure or function, such as myocytes function, skeletal muscle mass and strength, degree of muscle wasting or myopathies, among others.
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Funkenstein, Bruria, and Shaojun (Jim) Du. Interactions Between the GH-IGF axis and Myostatin in Regulating Muscle Growth in Sparus aurata. United States Department of Agriculture, March 2009. http://dx.doi.org/10.32747/2009.7696530.bard.

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Growth rate of cultured fish from hatching to commercial size is a major factor in the success of aquaculture. The normal stimulus for muscle growth in growing fish is not well understood and understanding the regulation of muscle growth in fish is of particular importance for aquaculture. Fish meat constitutes mostly of skeletal muscles and provides high value proteins in most people's diet. Unlike mammals, fish continue to grow throughout their lives, although the size fish attain, as adults, is species specific. Evidence indicates that muscle growth is regulated positively and negatively by a variety of growth and transcription factors that control both muscle cell proliferation and differentiation. In particular, growth hormone (GH), fibroblast growth factors (FGFs), insulin-like growth factors (IGFs) and transforming growth factor-13 (TGF-13) play critical roles in myogenesis during animal growth. An important advance in our understanding of muscle growth was provided by the recent discovery of the crucial functions of myostatin (MSTN) in controlling muscle growth. MSTN is a member of the TGF-13 superfamily and functions as a negative regulator of skeletal muscle growth in mammals. Studies in mammals also provided evidence for possible interactions between GH, IGFs, MSTN and the musclespecific transcription factor My oD with regards to muscle development and growth. The goal of our project was to try to clarify the role of MSTNs in Sparus aurata muscle growth and in particular determine the possible interaction between the GH-IGFaxis and MSTN in regulating muscle growth in fish. The steps to achieve this goal included: i) Determining possible relationship between changes in the expression of growth-related genes, MSTN and MyoD in muscle from slow and fast growing sea bream progeny of full-sib families and that of growth rate; ii) Testing the possible effect of over-expressing GH, IGF-I and IGF-Il on the expression of MSTN and MyoD in skeletal muscle both in vivo and in vitro; iii) Studying the regulation of the two S. aurata MSTN promoters and investigating the possible role of MyoD in this regulation. The major findings of our research can be summarized as follows: 1) Two MSTN promoters (saMSTN-1 and saMSTN-2) were isolated and characterized from S. aurata and were found to direct reporter gene activity in A204 cells. Studies were initiated to decipher the regulation of fish MSTN expression in vitro using the cloned promoters; 2) The gene coding for saMSTN-2 was cloned. Both the promoter and the first intron were found to be polymorphic. The first intron zygosity appears to be associated with growth rate; 3) Full length cDNA coding for S. aurata growth differentiation factor-l I (GDF-II), a closely related growth factor to MSTN, was cloned from S. aurata brain, and the mature peptide (C-terminal) was found to be highly conserved throughout evolution. GDF-II transcript was detected by RT -PCR analysis throughout development in S. aurata embryos and larvae, suggesting that this mRNA is the product of the embryonic genome. Transcripts for GDF-Il were detected by RT-PCR in brain, eye and spleen with highest level found in brain; 4) A novel member of the TGF-Bsuperfamily was partially cloned from S. aurata. It is highly homologous to an unidentified protein (TGF-B-like) from Tetraodon nigroviridisand is expressed in various tissues, including muscle; 5) Recombinant S. aurata GH was produced in bacteria, refolded and purified and was used in in vitro and in vivo experiments. Generally, the results of gene expression in response to GH administration in vivo depended on the nutritional state (starvation or feeding) and the time at which the fish were sacrificed after GH administration. In vitro, recombinantsaGH activated signal transduction in two fish cell lines: RTHI49 and SAFI; 6) A fibroblastic-like cell line from S. aurata (SAF-I) was characterized for its gene expression and was found to be a suitable experimental system for studies on GH-IGF and MSTN interactions; 7) The gene of the muscle-specific transcription factor Myogenin was cloned from S. aurata, its expression and promoter activity were characterized; 8) Three genes important to myofibrillogenesis were cloned from zebrafish: SmyDl, Hsp90al and skNAC. Our data suggests the existence of an interaction between the GH-IGFaxis and MSTN. This project yielded a great number of experimental tools, both DNA constructs and in vitro systems that will enable further studies on the regulation of MSTN expression and on the interactions between members of the GHIGFaxis and MSTN in regulating muscle growth in S. aurata.
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Walters, Thomas. Engineered Skeletal Muscle for Craniofacial Reconstruction. Fort Belvoir, VA: Defense Technical Information Center, November 2011. http://dx.doi.org/10.21236/ada601864.

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Yang, Hui, Xi-Xi Wan, Hui Ma, Zhen LI, Li Weng, Ying Xia, and Xiao-Ming Zhang. Prevalence and mortality risk of low skeletal muscle mass in critically ill patients: an updated systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0132.

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Review question / Objective: The PICOS principle was adopted when we confirmed the study eligibility. The inclusion criteria were as follows: (1) patients were critically ill, which was defined as adult patients who were from the ICU department; (2) exposure: patients had a clear definition of LSMM based on CT scans, anthropometric methods and ultrasound; (3) presented the prevalence of LSMM or could be calculated by the available data from the article; and (4) study design: observational study (cohort study or cross-sectional study). Articles that were reviews, case reports, comments, correspondences, letters or only abstracts were excluded. Condition being studied: Critical illness often results in low skeletal muscle mass for multiple reasons. Multiple studies have explored the association between low skeletal muscle mass and mortality. The prevalence of low skeletal muscle mass and its association with mortality are unclear. This systematic review and meta-analysis aim to identify the prevalence and mortality risk of low skeletal muscle mass among critically ill patients.
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Kuo, Meng-Hsuan, Chih-Wei Tseng, Ching-Sheng Hsu, Yen-Chun Chen, I.-Ting Kao, and Chen-Yi Wu. Protocol for systematic review and meta-analysis of prognostic value of sarcopenia in advanced HCC patients treating with systemic therapy. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0011.

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Review question / Objective: P: Advanced HCC patients under systemic therapy; I: low skeletal muscle mass (LSMM); C: Non-LSMM; O:overall survival or mortality. Eligibility criteria: (1) cohort studies or cross sectional studies investigations with HCC patients treated with systemic therapy; (2) the articles estimated pretreatment skeletal muscle mass measured by CT-images; (3) studies provided statistical data about the prevalence pretreatment LSMM or influence of LSMM on OS orPFS.
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Buck, Edmond. Mechanism of Calcium Release from Skeletal Muscle Sarcoplasmic Reticulum. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1306.

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Phillips, Stuart, Kyle Lau, Alysha D'Souza, and Everson Nunes. An umbrella review of systematic reviews of β-hydroxy-β-methyl butyrate (HMB) supplementation in promoting skeletal muscle mass and function in aging and clinical practice. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2021. http://dx.doi.org/10.37766/inplasy2021.10.0072.

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Review question / Objective: An umbrella review of systematic reviews of the use of β-hydroxy-β-methyl butyrate (HMB) supplementation in promoting skeletal muscle mass and function in aging and clinical practice. Condition being studied: Muscle mass (and various proxies thereof), strength, and physical function. Information sources: Pubmed, Web of Science, Embase.
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Geisler, Corinna, Mark Hübers, and Manfred Müller. Assessment of adult malnutrition with bioelectrical impedance analysis. Universitatsbibliothek Kiel, September 2018. http://dx.doi.org/10.21941/manueltask13.

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The two aims of this study were to evaluate (i) the prevalence of malnutrition based on age, sex and BMI specific PA and (ii) to determinate what specific body composition characteristics (skeletal muscle mass and adipose tissue) are related to a low PA.
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