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1
Gerçek, Cem. "Modelling the Subjects of Skeletal and Muscular System: Mobile Applications." Journal of Qualitative Research in Education 7, no. 1 (January 31, 2019): 1–16. http://dx.doi.org/10.14689/issn.2148-2624.1.7c1s.10m.
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2
Endo, Hiroshi, and Mitsuo Wada. "A Musculo-skeletal Mechanism Simulating Human Forearm and Its Control Method." Journal of Robotics and Mechatronics 5, no. 3 (June 20, 1993): 248–52. http://dx.doi.org/10.20965/jrm.1993.p0248.
Повний текст джерелаАнотація:
In the human muscular system, each muscle can regulate its compliance, all of the muscles act in opposition to each other, and certain muscles act on several joints. This mechanism serves for skillful human motions. To realize an improved manipulator, we implemented this mechanism into our manipulator which has a musculo-skeletal mechanism similar to a human forearm. The manipulator is driven by the tendon-driven system where the actions of the tendon-driven system are similar to those of the human muscular system. The manipulator has 2 D.O.F and is driven by three contending wires. In addition, the manipulator control method referring to the human muscular control system is investigated.
3
Schoenau, Eckhard. "Muscular System Is the Driver of Skeletal Development." Annales Nestlé (English ed.) 64, no. 2 (2006): 55–61. http://dx.doi.org/10.1159/000093012.
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4
Gimranova, Galina G., A. B. Bakirov, E. R. Shaikhlislamova, L. K. Karimova, N. A. Beigul, and L. N. Mavrina. "MUSCULO-SKELETAL AND PERIPHERAL NERVOUS DISEASES IN EMPLOYEES OF THE OIL INDUSTRY IN CONDITIONS OF THE COMBINED IMPACT OF VIBRATION AND THE HEAVY WORKING PROCESS." Hygiene and sanitation 96, no. 6 (March 27, 2019): 552–55. http://dx.doi.org/10.18821/0016-9900-2017-96-6-552-555.
Повний текст джерелаАнотація:
There were studied working conditions and the state of the muscular-skeletal system in employees of the oil industry. Working conditions of employees of basic occupations are referred to the hazard Class 3.1 - 3.3. Significant physical exertion with the predominant load on the lumbar-sacral area, constrained posture, the exposure to the general vibration and adverse weather conditions contribute to the development of diseases of the muscular-skeletal and peripheral nervous system. The most perspective trend in solving problems of diseases of the muscular-skeletal system is the implementation of the complex of preventive measures including both primary and secondary prophylaxis.
5
Akhtaruzzaman, M., A. A. Shafie, and M. R. Khan. "A REVIEW ON LOWER APPENDICULAR MUSCULOSKELETAL SYSTEM OF HUMAN BODY." IIUM Engineering Journal 17, no. 1 (April 30, 2016): 83–102. http://dx.doi.org/10.31436/iiumej.v17i1.571.
Повний текст джерелаАнотація:
Rehabilitation engineering plays an important role in designing various autonomous robots to provide better therapeutic exercise to disabled patients. Hence it is necessary to study human musculoskeletal system and also needs to be presented in scientific manner in order to describe and analyze the biomechanics of human body motion. This review focuses on lower appendicular musculoskeletal structure of human body to represent joints and links architectures; to identify muscle attachments and functions; and to illustrate muscle groups which are responsible for a particular joint movement. Firstly, human lower skeletal structure, linking systems, joint mechanisms, and their functions are described with a conceptual representation of joint architecture of human skeleton. This section also represents joints and limbs by comparing with mechanical systems. Characteristics of ligaments and their functions to construct skeletal joints are also discussed briefly in this part. Secondly, the study focuses on muscular system of human lower limbs where muscle structure, functions, roles in moving endoskeleton structure, and supporting mechanisms are presented elaborately. Thirdly, muscle groups are tabulated based on functions that provide mobility to different joints of lower limbs. Finally, for a particular movement action of lower extremity, muscles are also grouped and tabulated to have a better understanding on functions of individual muscle. Basically the study presents an overview of the structure of human lower limbs by characterizing and classifying skeletal and muscular systems.KEYWORDS: Â Musculoskeletal system; Human lower limbs; Muscle groups; Joint motion; Biomechatronics; Rehabilitation.
6
Staroseltseva, Natalia. "Muscular pain phenomena." Manual Therapy, no. 1 (May 3, 2022): 78–84. http://dx.doi.org/10.54504/1684-6753-2022-1-78-84.
Повний текст джерелаАнотація:
Noted was an apparent overdiagnosis of osteochondrosis as a major cause of pain syndrome, and along with it, underestimation of the role of functional disorders of the musculoskeletal system with the appearance of a reversible block in the small and large joints and the formation of musculo-skeletal pain syndromes. The main cause of back, neck and limb pain are myofascial pain syndromes, including manifestations of the fibro-myalgic syndrome.
7
Tripodi, Luana, Chiara Villa, Davide Molinaro, Yvan Torrente, and Andrea Farini. "The Immune System in Duchenne Muscular Dystrophy Pathogenesis." Biomedicines 9, no. 10 (October 11, 2021): 1447. http://dx.doi.org/10.3390/biomedicines9101447.
Повний текст джерелаАнотація:
Growing evidence demonstrates the crosstalk between the immune system and the skeletal muscle in inflammatory muscle diseases and dystrophic conditions such as Duchenne Muscular Dystrophy (DMD), as well as during normal muscle regeneration. The rising of inflammation and the consequent activation of the immune system are hallmarks of DMD: several efforts identified the immune cells that invade skeletal muscle as CD4+ and CD8+ T cells, Tregs, macrophages, eosinophils and natural killer T cells. The severity of muscle injury and inflammation dictates the impairment of muscle regeneration and the successive replacement of myofibers with connective and adipose tissue. Since immune system activation was traditionally considered as a consequence of muscular wasting, we recently demonstrated a defect in central tolerance caused by thymus alteration and the presence of autoreactive T-lymphocytes in DMD. Although the study of innate and adaptive immune responses and their complex relationship in DMD attracted the interest of many researchers in the last years, the results are so far barely exhaustive and sometimes contradictory. In this review, we describe the most recent improvements in the knowledge of immune system involvement in DMD pathogenesis, leading to new opportunities from a clinical point-of-view.
8
Powell, Jeanne A. "Muscular dysgenesis: a model system for studying skeletal muscle development." FASEB Journal 4, no. 10 (July 1990): 2798–808. http://dx.doi.org/10.1096/fasebj.4.10.2197156.
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9
Piróg, Katarzyna A., and Michael D. Briggs. "Skeletal Dysplasias Associated with Mild Myopathy—A Clinical and Molecular Review." Journal of Biomedicine and Biotechnology 2010 (2010): 1–13. http://dx.doi.org/10.1155/2010/686457.
Повний текст джерелаАнотація:
Musculoskeletal system is a complex assembly of tissues which acts as scaffold for the body and enables locomotion. It is often overlooked that different components of this system may biomechanically interact and affect each other. Skeletal dysplasias are diseases predominantly affecting the development of the osseous skeleton. However, in some cases skeletal dysplasia patients are referred to neuromuscular clinics prior to the correct skeletal diagnosis. The muscular complications seen in these cases are usually mild and may stem directly from the muscle defect and/or from the altered interactions between the individual components of the musculoskeletal system. A correct early diagnosis may enable better management of the patients and a better quality of life. This paper attempts to summarise the different components of the musculoskeletal system which are affected in skeletal dysplasias and lists several interesting examples of such diseases in order to enable better understanding of the complexity of human musculoskeletal system.
10
Golovskoy, B. V., M. D. Berg, I. A. Bulatova, E. I. Voronova, and Ya B. Khovaeva. "Muscular system in maintaining health and preventing chronic non-infectious diseases." Perm Medical Journal 38, no. 1 (April 22, 2021): 72–86. http://dx.doi.org/10.17816/pmj38172-86.
Повний текст джерелаАнотація:
Chronic non-infectious diseases are the leading cause of premature death according to the WHO data. This review considers the evolution of studying and modern views of domestic and foreign authors on the role of skeletal muscles in maintaining health and preventing chronic non-infectious diseases. An idea regarding the nervous and reflex influence from the working muscles on both individual organs and the body as a whole is presented. The role of myokines, specific proteins produced by skeletal muscles, capable of influencing the state of many organs and systems, is described.
11
Kalinin, R. E., I. A. Suchkov, N. D. Mzhavanadze, and N. V. Korotkova. "Endothelial dysfunction in muscular dystrophies." NAUKA MOLODYKH (Eruditio Juvenium) 9, no. 2 (June 30, 2021): 326–34. http://dx.doi.org/10.23888/hmj202192326-334.
Повний текст джерелаАнотація:
Endotheliocytes are the key elements of the vascular wall and are involved in regulation of vascular tone and permeability, inflammation, hemostasis, angiogenesis etc. Impaired function of endothelial cells universally recognized as endothelial dysfunction is associated with a number of common diseases such as ischemic heart disease, arterial hypertension, atherosclerosis, peripheral arterial disease, septic shock, chronic kidney disease, obesity, oncological and autoimmune diseases. Less is known about the role of endothelial cells in pathogenesis of development and progression of rare diseases, such as muscular dystrophies. Muscular dystrophies involve over 30 genetically determined diseases, which are characterized by the development of a progressive muscular weakness and skeletal muscle degeneration. Presence of a nucleotide variant associated with a certain muscular dystrophy is primarily marked by a limited potential of skeletal muscle regeneration due to the impaired structure and function of myogenic cells. Inherited myopathies include a group of severe neuromuscular diseases caused by a mutation in the dysferlin gene DYSF, which leads to the synthesis of a dysfunctional dysferlin. Complex molecular and cellular interactions involved in skeletal muscle damage and endothelial dysfunction play an important role in the pathogenesis of dysferlinopathies. The possibility to produce an effect on different pathological aspects of dysferlinassociated myopathies such as complement system activation, inflammation, impaired function of endothelial cells, damage and necrosis of myofibrils are extensively studied in vitro and in vivo. This article is dedicated to the current understanding of relationship between the endothelium and its dysfunction in myogenesis and skeletal muscle regeneration in normal and pathological conditions caused by a group of inherited progressive myodystrophies, dysferlinopathies in particular, as well as possible clinical application of endothelial cells in treatment of muscular dystrophies.
12
Chaitow, Leon. "The Muscular System Manual: The Skeletal Muscles of the Human Body." Journal of Bodywork and Movement Therapies 8, no. 1 (January 2004): 72. http://dx.doi.org/10.1016/s1360-8592(03)00059-7.
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13
Rahman, Fasih Ahmad, and Matthew Paul Krause. "PAI-1, the Plasminogen System, and Skeletal Muscle." International Journal of Molecular Sciences 21, no. 19 (September 25, 2020): 7066. http://dx.doi.org/10.3390/ijms21197066.
Повний текст джерелаАнотація:
The plasminogen system is a critical proteolytic system responsible for the remodeling of the extracellular matrix (ECM). The master regulator of the plasminogen system, plasminogen activator inhibitor-1 (PAI-1), has been implicated for its role in exacerbating various disease states not only through the accumulation of ECM (i.e., fibrosis) but also its role in altering cell fate/behaviour. Examination of PAI-1 has extended through various tissues and cell-types with recent investigations showing its presence in skeletal muscle. In skeletal muscle, the role of this protein has been implicated throughout the regeneration process, and in skeletal muscle pathologies (muscular dystrophy, diabetes, and aging-driven pathology). Needless to say, the complete function of this protein in skeletal muscle has yet to be fully elucidated. Given the importance of skeletal muscle in maintaining overall health and quality of life, it is critical to understand the alterations—particularly in PAI-1—that occur to negatively impact this organ. Thus, we provide a comprehensive review of the importance of PAI-1 in skeletal muscle health and function. We aim to shed light on the relevance of this protein in skeletal muscle and propose potential therapeutic approaches to aid in the maintenance of skeletal muscle health.
14
Granado, Miriam, Teresa Priego, Ana I. Martín, Mª Ángeles Villanúa, and Asunción López-Calderón. "Ghrelin receptor agonist GHRP-2 prevents arthritis-induced increase in E3 ubiquitin-ligating enzymes MuRF1 and MAFbx gene expression in skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 289, no. 6 (December 2005): E1007—E1014. http://dx.doi.org/10.1152/ajpendo.00109.2005.
Повний текст джерелаАнотація:
Chronic arthritis is a catabolic state associated with an inhibition of the IGF system and a decrease in body weight. Cachexia and muscular wasting is secondary to protein degradation by the ubiquitin-proteasome pathway. The aim of this work was to analyze the effect of adjuvant-induced arthritis on the muscle-specific ubiquitin ligases muscle ring finger 1 ( MuRF1) and muscle atrophy F-box ( MAFbx) as well as on IGF-I and IGF-binding protein-5 ( IGFBP-5) gene expression in the skeletal muscle. We also studied whether the synthetic ghrelin receptor agonist, growth hormone releasing peptide-2 (GHRP-2), was able to prevent arthritis-induced changes in the skeletal muscle. Arthritis induced an increase in MuRF1, MAFbx ( P < 0.01), and tumor necrosis factor ( TNF)-α mRNA ( P < 0.05) in the skeletal muscle. Arthritis decreased the serum IGF-I and its gene expression in the liver ( P < 0.01), whereas it increased IGF-I and IGFBP-5 gene expression in the skeletal muscle ( P < 0.01). Administration of GHRP-2 for 8 days prevented the arthritis-induced increase in muscular MuRF1, MAFbx, and TNF-α gene expression. GHRP-2 treatment increased the serum concentrations of IGF-I and the IGF-I mRNA in the liver and in the cardiac muscle and decreased muscular IGFBP-5 mRNA both in control and in arthritic rats ( P < 0.05). GHRP-2 treatment increased muscular IGF-I mRNA in control rats ( P < 0.01), but it did not modify the muscular IGF-I gene expression in arthritic rats. These data indicate that arthritis induces an increase in the activity of the ubiquitin-proteasome proteolytic pathway that is prevented by GHRP-2 administration. The parallel changes in muscular IGFBP-5 and TNF-α gene expression with the ubiquitin ligases suggest that they can participate in skeletal muscle alterations during chronic arthritis.
15
Khabirov, R. A. "Muscular syndrome in patients with inflammatory and degenerative diseases of joints and vertebral column." Kazan medical journal 80, no. 2 (March 25, 1999): 113–16. http://dx.doi.org/10.17816/kazmj65368.
Повний текст джерелаАнотація:
The manifestations of muscular syndrome affecting the gravity and prediction of the disease take place in the most widespread and invalidizing rheumatic diseases: osteoarthrosis, rheumatoid arthritis and ankylosing spondylarthritis. Paraclinical studies showed heterogeneity of pathogenetic mechanisms in lesion of skeletal muscles in rheumatic diseases. The differentiated methods of the treatment of patients with osteoarthrosis, rheumatoid arthritis and ankylosing spondylarthritis taking into account the clinical picture and pathogenesis of muscular syndrome, as well as the diagnosis criteria and classification of muscular system lesion are suggested.
16
Suzuki, Naoki, Asaki Hattori, Mitsuhito Hayashibe, Yoshito Otake, Shigeyuki Suzuki, and Susumu Kobayashi. "4D analysis of skeletal and muscular system during locomotion using dynamic spatial video camera system." International Congress Series 1268 (June 2004): 1239. http://dx.doi.org/10.1016/j.ics.2004.03.317.
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17
Chikani, Viral, and Ken K. Y. Ho. "Action of GH on skeletal muscle function: molecular and metabolic mechanisms." Journal of Molecular Endocrinology 52, no. 1 (October 25, 2013): R107—R123. http://dx.doi.org/10.1530/jme-13-0208.
Повний текст джерелаАнотація:
Skeletal muscle is a target tissue of GH. Based on its anabolic properties, it is widely accepted that GH enhances muscle performance in sports and muscle function in the elderly. This paper critically reviews information on the effects of GH on muscle function covering structure, protein metabolism, the role of IGF1 mediation, bioenergetics and performance drawn from molecular, cellular and physiological studies on animals and humans. GH increases muscle strength by enhancing muscle mass without affecting contractile force or fibre composition type. GH stimulates whole-body protein accretion with protein synthesis occurring in muscular and extra-muscular sites. The energy required to power muscle function is derived from a continuum of anaerobic and aerobic sources. Molecular and functional studies provide evidence that GH stimulates the anaerobic and suppresses the aerobic energy system, in turn affecting power-based functional measures in a time-dependent manner. GH exerts complex multi-system effects on skeletal muscle function in part mediated by the IGF system.
18
Gamucci, Fiorenza, Marcello Pallante, Sybille Molle, Enrico Merlo, and Andrea Bertuglia. "A Preliminary Study on the Use of HD-sEMG for the Functional Imaging of Equine Superficial Muscle Activation during Dynamic Mobilization Exercises." Animals 12, no. 6 (March 20, 2022): 785. http://dx.doi.org/10.3390/ani12060785.
Повний текст джерелаАнотація:
Superficial skeletal muscle activation is associated with an electric activity. Bidimensional High-Density Surface Electromyography (HD-sEMG) is a non-invasive technique that uses a grid of equally spaced electrodes applied on the skin surface to detect and portray superficial skeletal muscle activation. The goal of the study was to evaluate the feasibility of HD-sEMG to detect electrical activation of skeletal muscle and its application during rehabilitation exercises in horses. To fulfil this aim, activation of the superficial descending pectoral and external abdominal oblique core muscles were measured using HD-sEMG technology during dynamic mobilization exercises to induce lateral bending and flexion/extension tasks of the trunk. Masseter muscle was instrumented during mastication as a control condition. A 64 surface EMG channel wireless system was used with a single 64 electrode grid or a pair of 32 electrode grids. HD-sEMG provided unique information on the muscular activation onset, duration, and offset, along each motor task, and permitting inferences about the motor control strategy actuated by the central nervous system. Signals were further processed to obtain firing frequencies of few motor-neurons. Estimation of electromyographic amplitude and spectral parameters allowed detecting the onset of muscular fatigue during the motor tasks performed. HD-sEMG allows the assessment of muscular activation in horses performing specific motor tasks, supporting its future application in clinical and research settings.
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Ohlendorf, Daniela, Yvonne Haas, Antonia Naser, Jasmin Haenel, Laura Maltry, Fabian Holzgreve, Christina Erbe, et al. "Prevalence of Muscular Skeletal Disorders among Qualified Dental Assistants." International Journal of Environmental Research and Public Health 17, no. 10 (May 16, 2020): 3490. http://dx.doi.org/10.3390/ijerph17103490.
Повний текст джерелаАнотація:
The occupation of dental assistants (DAs) involves many health risks of the musculoskeletal system due to static and prolonged work, which can lead to musculoskeletal disorders (MSDs). The aim of the study was to investigate the prevalence of MSDs in DAs in Germany. Methods: For this purpose, an online questionnaire analyzed 406 (401 female participants and 5 male participants, 401w/5m) DAs. It was based on the Nordic Questionnaire (lifetime, 12-month, and seven-day MSDs’ prevalence separated into neck, shoulder, elbow, wrist, upper back, lower back, hip, knee, and ankle), and occupational and sociodemographic questions as well as questions about specific medical conditions. Results: 98.5% of the participants reported complaints of at least one body region in their lives, 97.5% reported at least one complaint in the last 12 months and 86.9% affirmed at least one complaint in the last seven days. For lifetime, 12-month and seven-day prevalence, the neck was the region that was most affected followed by the shoulder, the upper back and the lower back. Conclusion: The prevalence of MSDs among German (female) DAs was very high. The most affected area is the neck, followed by the shoulder, the lower back, and the upper back. It, therefore, seems necessary to devote more attention to ergonomics at the working practice of DAs as well in education and in dental work.
20
Coles, Chantal A., Ian Woodcock, Daniel G. Pellicci, and Peter J. Houweling. "A Spotlight on T Lymphocytes in Duchenne Muscular Dystrophy—Not Just a Muscle Defect." Biomedicines 10, no. 3 (February 24, 2022): 535. http://dx.doi.org/10.3390/biomedicines10030535.
Повний текст джерелаАнотація:
The lack of dystrophin in Duchenne muscular dystrophy (DMD) results in membrane fragility resulting in contraction-induced muscle damage and subsequent inflammation. The impact of inflammation is profound, resulting in fibrosis of skeletal muscle, the diaphragm and heart, which contributes to muscle weakness, reduced quality of life and premature death. To date, the innate immune system has been the major focus in individuals with DMD, and our understanding of the adaptive immune system, specifically T cells, is limited. Targeting the immune system has been the focus of multiple clinical trials for DMD and is considered a vital step in the development of better treatments. However, we must first have a complete picture of the involvement of the immune systems in dystrophic muscle disease to better understand how inflammation influences disease progression and severity. This review focuses on the role of T cells in DMD, highlighting the importance of looking beyond skeletal muscle when considering how the loss of dystrophin impacts disease progression. Finally, we propose that targeting T cells is a potential novel therapeutic in the treatment of DMD.
21
Ábrigo, Johanna, Alvaro A. Elorza, Claudia A. Riedel, Cristian Vilos, Felipe Simon, Daniel Cabrera, Lisbell Estrada, and Claudio Cabello-Verrugio. "Role of Oxidative Stress as Key Regulator of Muscle Wasting during Cachexia." Oxidative Medicine and Cellular Longevity 2018 (2018): 1–17. http://dx.doi.org/10.1155/2018/2063179.
Повний текст джерелаАнотація:
Skeletal muscle atrophy is a pathological condition mainly characterized by a loss of muscular mass and the contractile capacity of the skeletal muscle as a consequence of muscular weakness and decreased force generation. Cachexia is defined as a pathological condition secondary to illness characterized by the progressive loss of muscle mass with or without loss of fat mass and with concomitant diminution of muscle strength. The molecular mechanisms involved in cachexia include oxidative stress, protein synthesis/degradation imbalance, autophagy deregulation, increased myonuclear apoptosis, and mitochondrial dysfunction. Oxidative stress is one of the most common mechanisms of cachexia caused by different factors. It results in increased ROS levels, increased oxidation-dependent protein modification, and decreased antioxidant system functions. In this review, we will describe the importance of oxidative stress in skeletal muscles, its sources, and how it can regulate protein synthesis/degradation imbalance, autophagy deregulation, increased myonuclear apoptosis, and mitochondrial dysfunction involved in cachexia.
22
Waldrop, T. G., and J. H. Mitchell. "Effects of barodenervation on cardiovascular responses to static muscular contraction." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 4 (October 1, 1985): H710—H714. http://dx.doi.org/10.1152/ajpheart.1985.249.4.h710.
Повний текст джерелаАнотація:
The purpose of this study was to measure blood flow to various tissues during static muscular contraction in anesthetized cats and to evaluate if the baroreflex modulates the cardiovascular responses to muscular contraction. Contraction of the hindlimb muscles induced by ventral root stimulation caused increases in arterial pressure (delta 37.8 +/- 5.5 mmHg) and heart rate (delta 13.9 +/- 3.1 beats/min). Increases in blood flow to the heart, working skeletal muscles, and selected areas of the central nervous system occurred during muscular contraction. Blood flow to visceral organs did not change during muscular contraction. Baroreceptor-denervated cats showed a greater rise in arterial pressure (delta 55.5 +/- 5.5 mmHg) during muscular contraction than did the baroreceptor-intact cats. However, blood flow responses were similar in both groups. Thus the baroreceptor reflex modulates the pressor response without changing the alteration in blood flow during induced muscular contraction in anesthetized cats.
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dos Santos, Leandro, Alex Ribeiro, Edilaine Cavalcante, Hellen Nabuco, Melissa Antunes, Brad Schoenfeld, and Edilson Cyrino. "Effects of Modified Pyramid System on Muscular Strength and Hypertrophy in Older Women." International Journal of Sports Medicine 39, no. 08 (June 26, 2018): 613–18. http://dx.doi.org/10.1055/a-0634-6454.
Повний текст джерелаАнотація:
AbstractThis study aimed to analyze the effects of a pyramid system performed with two repetition zones on muscular strength and skeletal muscle mass (SMM) in older women. Thirty-nine physically independent older women (67.8±5.4 years) were randomly assigned into one of two of groups that performed an 8-week resistance training program in an ascending pyramid fashion. Both groups performed 3 sets: a narrow repetition zone (NPR, n=20) with 12/10/8 repetitions, and a wide repetition zone (WPR, n=19) with 15/10/5 repetitions. The program consisted of 8 whole-body exercises, performed 3 times a week. Dual-energy X-ray absorptiometry was used to measure SMM, and muscular strength was evaluated by one-repetition maximum (1RM). Both groups increased (P<0.05) SMM (NPR=+ 4.7%, effect size=+ 0.34; WPR=+ 8.4%, effect size=+ 0.77), and total strength (NPR=+ 11.3%, effect size=+ 0.80; WPR=+ 13.8%, effect size=0.84), without statistical differences between them. Results suggest that both zones of repetitions in a pyramid system are effective strategies to improve muscular strength and muscle growth in older women.
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IVANCEVIC, VLADIMIR. "LIE–LAGRANGIAN MODEL FOR REALISTIC HUMAN BIODYNAMICS." International Journal of Humanoid Robotics 03, no. 02 (June 2006): 205–18. http://dx.doi.org/10.1142/s0219843606000680.
Повний текст джерелаАнотація:
We present a sophisticated Lagrangian model for anatomically and physiologically realistic human biodynamics (RHB), to accompany the recently reported Hamiltonian formulation.1 The present RHB formulation is designed around three main modules: (i) A Riemannian configuration manifold, composed of gauge Lie groups of constrained 3D rotations and translations, which includes more than 300 degrees of freedom (DOF); (ii) exterior Lagrangian dynamics of the human musculo-skeletal system, including all natural conservative, dissipative and driving forces, powered by 600 equivalent muscles; and (iii) hierarchical nonlinear control, based on an iterative Lie derivative formalism, resembling both spinal reflexes and coordination-control of the human cerebellum. RHB is driven by individual, user supplied musculo-skeletal data. It is modeled in the computer algebra system Mathematica™, simulated in Delphi™ and animated in the 3DS Max™ graphical environment. As an applied example of RHB, we present the full spine simulator, with 150 DOF (25 movable joints each with three constrained rotations and translations), muscular excitation and contraction dynamics, spring-and-damper ligament-like dynamics, spinal-like and cerebellar-like control, and external torques and forces (including inertial, gravitational, viscous, elastic and various types of impacts).
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Mosca, Nicola, Sara Petrillo, Sara Bortolani, Mauro Monforte, Enzo Ricci, Fiorella Piemonte, and Giorgio Tasca. "Redox Homeostasis in Muscular Dystrophies." Cells 10, no. 6 (June 1, 2021): 1364. http://dx.doi.org/10.3390/cells10061364.
Повний текст джерелаАнотація:
In recent years, growing evidence has suggested a prominent role of oxidative stress in the pathophysiology of several early- and adult-onset muscle disorders, although effective antioxidant treatments are still lacking. Oxidative stress causes cell damage by affecting protein function, membrane structure, lipid metabolism, and DNA integrity, thus interfering with skeletal muscle homeostasis and functionality. Some features related to oxidative stress, such as chronic inflammation, defective regeneration, and mitochondrial damage are shared among most muscular dystrophies, and Nrf2 has been shown to be a central player in antagonizing redox imbalance in several of these disorders. However, the exact mechanisms leading to overproduction of reactive oxygen species and deregulation in the cellular antioxidants system seem to be, to a large extent, disease-specific, and the clarification of these mechanisms in vivo in humans is the cornerstone for the development of targeted antioxidant therapies, which will require testing in appropriately designed clinical trials.
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Cartier, L. J., and P. D. Gollnick. "Sympathoadrenal system and activation of glycogenolysis during muscular activity." Journal of Applied Physiology 58, no. 4 (April 1, 1985): 1122–27. http://dx.doi.org/10.1152/jappl.1985.58.4.1122.
Повний текст джерелаАнотація:
Comparisons were made of the appearance of phosphorylase (PHOS) a and lactate (LA) during electrical stimulation of the gastrocnemius (GM) and soleus (SM) muscles of normal and sympathectomized (SYMPX) rats. Ten-second stimulation at 3 Hz increased PHOS a approximately fourfold in the GM of normal rats, whereafter it declined during stimulation until at 60 s it was similar to rest. The increase in PHOS a of GM from SYMPX rats after 10 s of stimulation was approximately 50% that of normal rats. Stimulation of the SM produced smaller and slower increases in PHOS a with the peak occurring after 60 s, which remained constant to 90 s. SYMPX did not alter this effect in the SM. LA production and creatine phosphate depletion in the GM were continuous throughout stimulation and uninfluenced by SYMPX. This was true for the SM with the exception of LA production being greater after SYMPX. [ATP] was unchanged by electrical stimulation. The rate and magnitude of the PHOS a appearance was a function of stimulation frequency. Reversion of PHOS to the b form after stimulation was rapid, with approximately 50% of the peak value being attained in 2.5 s, and at 5 s the values were those of rest. These data demonstrate that an intact sympathoadrenal system is not obligatory for the initiation of glycogenolysis in skeletal muscle.
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Ching Sia, Lim, Maharshi Dave, Jagdish Prasad Sharma, and Tyrus A. McCarty. "Stability Analysis of Muscular and Skeletal System of Human’s leg segments (Thigh and Shank)." International Journal of Darshan Institute on Engineering Research & Emerging Technology 9, no. 1 (September 9, 2020): 1–8. http://dx.doi.org/10.32692/ijdi-eret/9.1.2020.2001.
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Schönau, Eckhard. "The Development of the Skeletal System in Children and the Influence of Muscular Strength." Hormone Research in Paediatrics 49, no. 1 (December 16, 1997): 27–31. http://dx.doi.org/10.1159/000023122.
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Lezhenko, G., O. Pashkova, K. Samoylyk, and A. Brutman. "Functional and biochemical characteristics of the muscle system in children with type I diabetes." CHILD`S HEALTH 17, no. 5 (October 18, 2022): 249–55. http://dx.doi.org/10.22141/2224-0551.17.5.2022.1525.
Повний текст джерелаАнотація:
Background. The purpose of the study was to determine possible markers of skeletal muscle damage in children with type 1 diabetes mellitus (T1DM) and their relationship with the features of disease course. Materials and methods. The observation group consisted of 98 children with type 1 diabetes mellitus: the first group included 22 people without disorders of the muscular system; the second — 42 patients with dynapenia; the third — 34 children with diabetic myopathy. Control group — 30 relatively healthy children. Assessment of the static endurance of skeletal muscles, determination of the level of creatine kinase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase, periostin and cardiotrophin-1 in blood serum were performed in all patients. Results. The conducted studies demonstrate that children with diabetes, regardless of the structural and functional state of their muscular system, have signs of skeletal muscle damage, which were most expressed in diabetic myopathy and progressed with maximal deterioration of glycemic control. It was found that the highest content of alkaline phosphatase was characteristic of children from group 1, while in patients with diabetic myopathy its serum content was not statistically different from that of controls. These disorders occurred against the background of changes in alkaline phosphatase activity, the level of which was highest in children from group 1, while in patients with diabetic myopathy, its serum content was not statistically different from that of controls. At the same time, during the course of diabetic myopathy in children with T1DM, there was an increase in lactate dehydrogenase activity by 1.2 times (p < 0.01) and cardiotrophin-1 by 300 times (p < 0.01) compared to the corresponding indicator of the control group. Serum periostin level was increased in all patients with T1DM. Its maximum values were determined in group 1, whose periostin concentration exceeded control indicators by 103 times (p < 0.01). With deterioration of skeletal muscle state, there was a gradual decrease in periostin serum level, but in patients with dynapenia, it was 35.5 times higher than in the control group (p < 0.05) and 19.2 times higher in those with diabetic myopathy (p < 0.05). Conclusions. The course of type 1 diabetes in children is accompanied by skeletal muscle damage, the first clinical sign of which is a decrease in the static muscle endurance against the background of worsening disease course. Alkaline phosphatase, lactate dehydrogenase, periostin, and cardiotrophin-1 are biochemical markers of skeletal muscle damage in children with type 1 diabetes. A common feature of the changes in the specified indicators is their increase; however, each clinical condition of the skeletal muscles corresponds to its own configuration of changes in the abovementioned markers.
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Aizawa, Katsuji, Motoyuki Iemitsu, Takeshi Otsuki, Seiji Maeda, Takashi Miyauchi, and Noboru Mesaki. "Sex differences in steroidogenesis in skeletal muscle following a single bout of exercise in rats." Journal of Applied Physiology 104, no. 1 (January 2008): 67–74. http://dx.doi.org/10.1152/japplphysiol.00558.2007.
Повний текст джерелаАнотація:
Sex steroid hormones, such as testosterone and estradiol, play important roles in developing both strength and mass of skeletal muscle. Recently, we demonstrated that skeletal muscle can synthesize sex steroid hormones. Whether there are sex differences in basal steroidogenesis or acute exercise-induced alterations of steroidogenesis in the skeletal muscle is unknown. We examined sex differences in the levels of testosterone, estradiol, and steroidogenesis-related enzymes, such as 17β-hydroxysteroid dehydrogenase (HSD), 3β-HSD, and aromatase cytochrome P-450 (P450arom), in the skeletal muscle at rest and after exercise. We studied the gastrocnemius muscles of resting rats (10 wk old) and exercised rats (10 wk old, treadmill running, 30 m/min, 30 min). Basal muscular testosterone levels were higher in males than females, whereas estradiol did not differ between sexes. Additionally, 17β-HSD, 3β-HSD, and P450arom transcript and protein expression were greater in females. After acute exercise, testosterone levels and 17β-HSD expression increased in muscle in both sexes. By comparison, muscular estradiol levels increased in males following exercise but were unchanged in females. Expression of P450arom, which regulates estrogen synthesis, increased after acute exercise in males but decreased after exercise in females. Thus a single bout of exercise can influence the steroidogenic system in skeletal muscle, and these alterations differ between sexes. The acute exercise-induced alteration of steroidogenic enzymes may enhance the local steroidogenesis in the skeletal muscle in both sexes.
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Khairullin, Adel E., Sergey N. Grishin, and Ayrat U. Ziganshin. "P2 Receptor Signaling in Motor Units in Muscular Dystrophy." International Journal of Molecular Sciences 24, no. 2 (January 13, 2023): 1587. http://dx.doi.org/10.3390/ijms24021587.
Повний текст джерелаАнотація:
The purine signaling system is represented by purine and pyrimidine nucleotides and nucleosides that exert their effects through the adenosine, P2X and P2Y receptor families. It is known that, under physiological conditions, P2 receptors play only a minor role in modulating the functions of cells and systems; however, their role significantly increases under some pathophysiological conditions, such as stress, ischemia or hypothermia, when they can play a dominant role as a signaling molecule. The diversity of P2 receptors and their wide distribution in the body make them very attractive as a target for the pharmacological action of drugs with a new mechanism of action. The review is devoted to the involvement of P2 signaling in the development of pathologies associated with a loss of muscle mass. The contribution of adenosine triphosphate (ATP) as a signal molecule in the pathogenesis of a number of muscular dystrophies (Duchenne, Becker and limb girdle muscular dystrophy 2B) is considered. To understand the processes involving the purinergic system, the role of the ATP and P2 receptors in several models associated with skeletal muscle degradation is also discussed.
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Arora, Shivani, and Chirag Arora. "A REVIEW ON CONCEPTUAL STUDY OF MUSCULAR DYSTROPHIES: AN AYURVEDIC PERSPECTIVE." International Journal of Research in Ayurveda and Pharmacy 13, no. 01 (February 23, 2022): 92–95. http://dx.doi.org/10.7897/2277-4343.130121.
Повний текст джерелаАнотація:
Muscular dystrophies (M.D.) are a category of hereditary illnesses defined by degeneration of the skeletal muscles that control mobility, culminating in muscle atrophy, weakness, confinement to a wheelchair, and eventually death. The most common muscular dystrophy is Duchenne muscular dystrophy (DMD), caused by a lack of the dystrophin gene. In Ayurvedic scriptures, muscular dystrophy is not explicitly linked to any ailment. The notion of Adibala pravritta vyadhi in Ayurveda helps to explain this aetiology. Pathogenesis occurs here due to Beejobhagavayava dushti, which leads to Mamsa Vata dushti. Because there is no specific treatment for muscle dystrophies in any medical system, the modern therapeutic approach of M.D is corticosteroids, physical therapy, respiratory assistance and gene therapy. In muscular dystrophy patients, Ayurvedic treatments such as Santarpana chikitsa, a collection of herbo-mineral medications, and specific Panchkarma therapies have an apparent protective effect and a prolonged survival rate. The current review article discusses the notion of muscular dystrophy from an Ayurvedic perspective and treatments and drugs that can help with the disease.
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Al-Sabri, Mohamed H., Neha Behare, Ahmed M. Alsehli, Samuel Berkins, Aadeya Arora, Eirini Antoniou, Eleni I. Moysiadou, et al. "Statins Induce Locomotion and Muscular Phenotypes in Drosophila melanogaster That Are Reminiscent of Human Myopathy: Evidence for the Role of the Chloride Channel Inhibition in the Muscular Phenotypes." Cells 11, no. 22 (November 8, 2022): 3528. http://dx.doi.org/10.3390/cells11223528.
Повний текст джерелаАнотація:
The underlying mechanisms for statin-induced myopathy (SIM) are still equivocal. In this study, we employ Drosophila melanogaster to dissect possible underlying mechanisms for SIM. We observe that chronic fluvastatin treatment causes reduced general locomotion activity and climbing ability. In addition, transmission microscopy of dissected skeletal muscles of fluvastatin-treated flies reveals strong myofibrillar damage, including increased sarcomere lengths and Z-line streaming, which are reminiscent of myopathy, along with fragmented mitochondria of larger sizes, most of which are round-like shapes. Furthermore, chronic fluvastatin treatment is associated with impaired lipid metabolism and insulin signalling. Mechanistically, knockdown of the statin-target Hmgcr in the skeletal muscles recapitulates fluvastatin-induced mitochondrial phenotypes and lowered general locomotion activity; however, it was not sufficient to alter sarcomere length or elicit myofibrillar damage compared to controls or fluvastatin treatment. Moreover, we found that fluvastatin treatment was associated with reduced expression of the skeletal muscle chloride channel, ClC-a (Drosophila homolog of CLCN1), while selective knockdown of skeletal muscle ClC-a also recapitulated fluvastatin-induced myofibril damage and increased sarcomere lengths. Surprisingly, exercising fluvastatin-treated flies restored ClC-a expression and normalized sarcomere lengths, suggesting that fluvastatin-induced myofibrillar phenotypes could be linked to lowered ClC-a expression. Taken together, these results may indicate the potential role of ClC-a inhibition in statin-associated muscular phenotypes. This study underlines the importance of Drosophila melanogaster as a powerful model system for elucidating the locomotion and muscular phenotypes, promoting a better understanding of the molecular mechanisms underlying SIM.
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K, Sathyavikasini, and Vijaya M S. "Identification of Rare Genetic Disorder from Single Nucleotide Variants Using Supervised Learning Technique." IAES International Journal of Artificial Intelligence (IJ-AI) 6, no. 4 (December 1, 2017): 174. http://dx.doi.org/10.11591/ijai.v6.i4.pp174-184.
Повний текст джерелаАнотація:
Muscular dystrophy is a rare genetic disorder that affects the muscular system which deteriorates the skeletal muscles and hinders locomotion. In the finding of genetic disorders such as Muscular dystrophy, the disease is identified based on mutations in the gene sequence. A new model is proposed for classifying the disease accurately using gene sequences, mutated by adopting positional cloning on the reference cDNA sequence. The features of mutated gene sequences for missense, nonsense and silent mutations aims in distinguishing the type of disease and the classifiers are trained with commonly used supervised pattern learning techniques.10-fold cross validation results show that the decision tree algorithm was found to attain the best accuracy of 100%. In summary, this study provides an automatic model to classify the muscular dystrophy disease and shed a new light on predicting the genetic disorder from gene based features through pattern recognition model.
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Volonte, Daniela, Aaron J. Peoples, and Ferruccio Galbiati. "Modulation of Myoblast Fusion by Caveolin-3 in Dystrophic Skeletal Muscle Cells: Implications for Duchenne Muscular Dystrophy and Limb-Girdle Muscular Dystrophy-1C." Molecular Biology of the Cell 14, no. 10 (October 2003): 4075–88. http://dx.doi.org/10.1091/mbc.e03-03-0161.
Повний текст джерелаАнотація:
Caveolae are vesicular invaginations of the plasma membrane. Caveolin-3 is the principal structural component of caveolae in skeletal muscle cells in vivo. We have recently generated caveolin-3 transgenic mice and demonstrated that overexpression of wild-type caveolin-3 in skeletal muscle fibers is sufficient to induce a Duchenne-like muscular dystrophy phenotype. In addition, we have shown that caveolin-3 null mice display mild muscle fiber degeneration and T-tubule system abnormalities. These data are consistent with the mild phenotype observed in Limb-girdle muscular dystrophy-1C (LGMD-1C) in humans, characterized by a ∼95% reduction of caveolin-3 expression. Thus, caveolin-3 transgenic and null mice represent valid mouse models to study Duchenne muscular dystrophy (DMD) and LGMD-1C, respectively, in humans. Here, we derived conditionally immortalized precursor skeletal muscle cells from caveolin-3 transgenic and null mice. We show that overexpression of caveolin-3 inhibits myoblast fusion to multinucleated myotubes and lack of caveolin-3 enhances the fusion process. M-cadherin and microtubules have been proposed to mediate the fusion of myoblasts to myotubes. Interestingly, we show that M-cadherin is downregulated in caveolin-3 transgenic cells and upregulated in caveolin-3 null cells. For the first time, variations of M-cadherin expression have been linked to a muscular dystrophy phenotype. In addition, we demonstrate that microtubules are disorganized in caveolin-3 null myotubes, indicating the importance of the cytoskeleton network in mediating the phenotype observed in these cells. Taken together, these results propose caveolin-3 as a key player in myoblast fusion and suggest that defects of the fusion process may represent additional molecular mechanisms underlying the pathogenesis of DMD and LGMD-1C in humans.
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Hammerer-Lercher, Angelika, Petra Erlacher, Reginald Bittner, Rudolf Korinthenberg, Daniela Skladal, Stephan Sorichter, Wolfgang Sperl, Bernd Puschendorf, and Johannes Mair. "Clinical and Experimental Results on Cardiac Troponin Expression in Duchenne Muscular Dystrophy." Clinical Chemistry 47, no. 3 (March 1, 2001): 451–58. http://dx.doi.org/10.1093/clinchem/47.3.451.
Повний текст джерелаАнотація:
Abstract Background: Because of controversial earlier studies, the purpose of this study was to provide novel experimental and additional clinical data regarding the possible reexpression of cardiac troponin T (cTnT) in regenerating skeletal muscle in Duchenne muscular dystrophy (DMD). Methods: Plasma from 14 patients (mean age, 7.5 years; range, 5.7–19.4 years) with DMD was investigated for creatine kinase (CK), the CK MB isoenzyme (CKMB), cTnT and cardiac troponin I (cTnI), and myoglobin. cTnT concentrations were measured by an ELISA (second-generation assay; Roche) using the ES 300 Analyzer. cTnI, myoglobin, and CKMB were measured by an ELISA using the ACCESS System (Beckman Diagnostics). Troponin isoform expression was studied by Western blot analysis in remnants of skeletal muscle biopsies of three patients with DMD and in an animal model of DMD (mdx mice; n = 6). Results: There was no relation of cTnT and cTnI to clinical evidence for cardiac failure. cTnI concentrations remained below the upper reference limit in all patients. cTnT was increased (median, 0.11 μg/L; range, 0.06–0.16 μg/L) in 50% of patients. The only significant correlation was found for CK (median, 3938 U/L; range, 2763–5030 U/L) with age (median, 7.5 years; range, 6.8–10.9 years; r = −0.762; P = 0.042). Western blot analysis of human or mouse homogenized muscle specimens showed no evidence for cardiac TnT and cTnI expression, despite strong signals for skeletal muscle troponin isoforms. Conclusions: We found no evidence for cTnT reexpression in human early-stage DMD and in mdx mouse skeletal muscle biopsies. Discrepancies of cTnT and cTnI in plasma samples of DMD patients were found, but neither cTnT nor cTnI plasma concentrations were related with other clinical evidence for cardiac involvement.
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Lin, Hwai-Ting, Yasuo Nakamura, Fong-Chin Su, Jun Hashimoto, Katsuya Nobuhara, and Edmund Y. S. Chao. "Use of Virtual, Interactive, Musculoskeletal System (VIMS) in Modeling and Analysis of Shoulder Throwing Activity." Journal of Biomechanical Engineering 127, no. 3 (January 1, 2005): 525–30. http://dx.doi.org/10.1115/1.1894387.
Повний текст джерелаАнотація:
Our purpose in this study was to apply the virtual, interactive, musculoskeletal system (VIMS) software for modeling and biomechanical analysis of the glenohumeral joint during a baseball pitching activity. The skeletal model was from VIMS library and muscle fiber attachment sites were derived from the visible human dataset. The muscular moment arms and function changes are mainly due to the large humeral motion involved during baseball pitching. The graphic animation of the anatomic system using VIMS software is an effective tool to model and visualize the complex anatomical structure of the shoulder for biomechanical analysis.
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Cifuentes-Diaz, Carmen, Tony Frugier, Francesco D. Tiziano, Emmanuelle Lacène, Natacha Roblot, Vandana Joshi, Marie Helene Moreau, and Judith Melki. "Deletion of Murine SMN Exon 7 Directed to Skeletal Muscle Leads to Severe Muscular Dystrophy." Journal of Cell Biology 152, no. 5 (March 5, 2001): 1107–14. http://dx.doi.org/10.1083/jcb.152.5.1107.
Повний текст джерелаАнотація:
Spinal muscular atrophy (SMA) is characterized by degeneration of motor neurons of the spinal cord associated with muscle paralysis and caused by mutations of the survival motor neuron gene (SMN). To determine whether SMN gene defect in skeletal muscle might have a role in SMA pathogenesis, deletion of murine SMN exon 7, the most frequent mutation found in SMA, has been restricted to skeletal muscle by using the Cre-loxP system. Mutant mice display ongoing muscle necrosis with a dystrophic phenotype leading to muscle paralysis and death. The dystrophic phenotype is associated with elevated levels of creatine kinase activity, Evans blue dye uptake into muscle fibers, reduced amount of dystrophin and upregulation of utrophin expression suggesting a destabilization of the sarcolemma components. The mutant mice will be a valuable model for elucidating the underlying mechanism. Moreover, our results suggest a primary involvement of skeletal muscle in human SMA, which may contribute to motor defect in addition to muscle denervation caused by the motor neuron degeneration. These data may have important implications for the development of therapeutic strategies in SMA.
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Lo Mauro, Antonella, and Andrea Aliverti. "Physiology of respiratory disturbances in muscular dystrophies." Breathe 12, no. 4 (November 30, 2016): 318–27. http://dx.doi.org/10.1183/20734735.012716.
Повний текст джерелаАнотація:
Muscular dystrophy is a group of inherited myopathies characterised by progressive skeletal muscle wasting, including of the respiratory muscles. Respiratory failure,i.e. when the respiratory system fails in its gas exchange functions, is a common feature in muscular dystrophy, being the main cause of death, and it is a consequence of lung failure, pump failure or a combination of the two. The former is due to recurrent aspiration, the latter to progressive weakness of respiratory muscles and an increase in the load against which they must contract. In fact, both the resistive and elastic components of the work of breathing increase due to airway obstruction and chest wall and lung stiffening, respectively.The respiratory disturbances in muscular dystrophy are restrictive pulmonary function, hypoventilation, altered thoracoabdominal pattern, hypercapnia, dyspnoea, impaired regulation of breathing, inefficient cough and sleep disordered breathing. They can be present at different rates according to the type of muscular dystrophy and its progression, leading to different onset of each symptom, prognosis and degree of respiratory involvement.Key pointsA common feature of muscular dystrophy is respiratory failure,i.e.the inability of the respiratory system to provide proper oxygenation and carbon dioxide elimination.In the lung, respiratory failure is caused by recurrent aspiration, and leads to hypoxaemia and hypercarbia.Ventilatory failure in muscular dystrophy is caused by increased respiratory load and respiratory muscles weakness.Respiratory load increases in muscular dystrophy because scoliosis makes chest wall compliance decrease, atelectasis and fibrosis make lung compliance decrease, and airway obstruction makes airway resistance increase.The consequences of respiratory pump failure are restrictive pulmonary function, hypoventilation, altered thoracoabdominal pattern, hypercapnia, dyspnoea, impaired regulation of breathing, inefficient cough and sleep disordered breathing.Educational aimsTo understand the mechanisms leading to respiratory disturbances in patients with muscular dystrophy.To understand the impact of respiratory disturbances in patients with muscular dystrophy.To provide a brief description of the main forms of muscular dystrophy with their respiratory implications.
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Sokołowska, Emilia, and Agnieszka Urszula Błachnio-Zabielska. "A Critical Review of Electroporation as A Plasmid Delivery System in Mouse Skeletal Muscle." International Journal of Molecular Sciences 20, no. 11 (June 6, 2019): 2776. http://dx.doi.org/10.3390/ijms20112776.
Повний текст джерелаАнотація:
The gene delivery to skeletal muscles is a promising strategy for the treatment of both muscular disorders (by silencing or overexpression of specific gene) and systemic secretion of therapeutic proteins. The use of a physical method like electroporation with plate or needle electrodes facilitates long-lasting gene silencing in situ. It has been reported that electroporation enhances the expression of the naked DNA gene in the skeletal muscle up to 100 times and decreases the changeability of the intramuscular expression. Coelectransfer of reporter genes such as green fluorescent protein (GFP), luciferase or beta-galactosidase allows the observation of correctly performed silencing in the muscles. Appropriate selection of plasmid injection volume and concentration, as well as electrotransfer parameters, such as the voltage, the length and the number of electrical pulses do not cause long-term damage to myocytes. In this review, we summarized the electroporation methodology as well as the procedure of electrotransfer to the gastrocnemius, tibialis, soleus and foot muscles and compare their advantages and disadvantages.
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Bailey, Donald A., and Alan D. Martin. "Physical Activity and Skeletal Health in Adolescents." Pediatric Exercise Science 6, no. 4 (November 1994): 330–47. http://dx.doi.org/10.1123/pes.6.4.330.
Повний текст джерелаАнотація:
A considerable amount of research into osteoporosis has focused on the management and treatment of bone loss in later life. More recently, a limited amount of research has been directed toward the development of an optimal level of peak bone mass during the adolescent and early adult years. While genetics is a major determinant of bone status, there is considerable evidence that physical activity is an important nonhereditary factor. Studies on adults suggest that the positive effect of physical activity on bone is modest in the short term but may be quite powerful with more intense activity that overloads the muscular system for a longer time period. In children, however, our knowledge about the long-term effects of physical activity on bone accretion is incomplete. This paper presents a review of the pediatric literature dealing with the relationship of physical activity to bone mineral density status in the adolescent population.
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Ackerly, Spafford C. "Mechanical couplings in the shell closing mechanism of articulate brachiopods: implications for the evolution of skeleto-muscular architecture." Paleobiology 19, no. 4 (1993): 420–32. http://dx.doi.org/10.1017/s0094837300014068.
Повний текст джерелаАнотація:
Rapid shell closure in articulate brachiopods occurs by a twitch contraction of the “quick” adductor muscles. Rapid accelerations and decelerations of the valves induce large accelerations of the surrounding fluid, placing constraints on the speeds of closure; inertial forces govern the mechanics of the closing mechanism. The position, size, and physiological properties of the muscles, and the size and shape of the shell, govern the properties of the shell closing system. A numerical model predicts that, for given muscle and shell characteristics, there is a location of the adductor muscle which maximizes the shell's closing velocity, and that this position shifts allometrically with size. Positive allometry in the muscle's moment arm length is observed in both living and fossil brachiopods, although the observed coefficients are less than those predicted by the model.The brachiopod closing mechanism provides a model for understanding the biomechanical interrelationships between components of dynamic skeletal systems. Dynamic systems, where the muscles induce resisting inertial reactions, are characterized by mechanical feedback loops, or couplings. Mechanical couplings may represent an important class of constraints on the evolution of skeleto-muscular architecture.
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Dalise, Stefania, Valentina Azzollini, and Carmelo Chisari. "Brain and Muscle: How Central Nervous System Disorders Can Modify the Skeletal Muscle." Diagnostics 10, no. 12 (December 4, 2020): 1047. http://dx.doi.org/10.3390/diagnostics10121047.
Повний текст джерелаАнотація:
It is widely known that nervous and muscular systems work together and that they are strictly dependent in their structure and functions. Consequently, muscles undergo macro and microscopic changes with subsequent alterations after a central nervous system (CNS) disease. Despite this, only a few researchers have addressed the problem of skeletal muscle abnormalities following CNS diseases. The purpose of this review is to summarize the current knowledge on the potential mechanisms responsible for changes in skeletal muscle of patients suffering from some of the most common CSN disorders (Stroke, Multiple Sclerosis, Parkinson’s disease). With this purpose, we analyzed the studies published in the last decade. The published studies show an extreme heterogeneity of the assessment modality and examined population. Furthermore, it is evident that thanks to different evaluation methodologies, it is now possible to implement knowledge on muscle morphology, for a long time limited by the requirement of muscle biopsies. This could be the first step to amplify studies aimed to analyze muscle characteristics in CNS disease and developing rehabilitation protocols to prevent and treat the muscle, often neglected in CNS disease.
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Vaz, Marco Aurélio, and Walter Herzog. "A MECANOGRAFIA COMO TÉCNICA NÃO-INVASIVA PARA O ESTUDO DA FUNÇÃO MUSCULAR." Movimento (ESEFID/UFRGS) 5, no. 10 (October 18, 2007): 15–20. http://dx.doi.org/10.22456/1982-8918.2450.
Повний текст джерелаАнотація:
A mecanomiografia (MMG) é uma técnica nao-invasiva que registra as vibrações ou sons produzidos pelo músculo esquelético ao se contrair. As primeiras observações da existência destas vibrações foi feita há mais de trezentos anos, mas limitações tecnológicas fizeram com que a MMG só recebesse atenção nas últimas décadas. A teoria mais aceita para explicar o mecanismo dessas vibrações é a de que elas são produzidas pela contração tetânica incompleta das unidades motoras. O sinal MMG fornece informações relativas aos padrões de ativação elétrica e ao comportamento mecânico do músculo. Essa técnica pode ser utilizada para estudar as propriedades mecânicas do sistema muscular, o controle motor, a fadiga muscular entre outras aplicações. Mecanomyography (MMG) is a non-invasive technique that records the vibrations or sounds produced by skeletal muscle during contraction. The first observations of the existence of these vibrations/sounds occurred more than three hundred years ago, but due to technological limitations the MMG only received attention in the last few decades. The most accepted theory to the mechanism of these vibrations is that they are produced by the unfused tetanic contraction of motor units. The MMG signal provides information related both to the activation patterns and to the mechanical behavior of skeletal muscle. This technique might be used to study the mechanical properties of the muscular system, motor control, muscle fatigue amongst other applications.
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Jarrah, Abdul Salam, Filippo Castiglione, Nicholas P. Evans, Robert W. Grange, and Reinhard Laubenbacher. "A Mathematical Model of Skeletal Muscle Disease and Immune Response in themdxMouse." BioMed Research International 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/871810.
Повний текст джерелаАнотація:
Duchenne muscular dystrophy (DMD) is a genetic disease that results in the death of affected boys by early adulthood. The genetic defect responsible for DMD has been known for over 25 years, yet at present there is neither cure nor effective treatment for DMD. During early disease onset, themdx mousehas been validated as an animal model for DMD and use of this model has led to valuable but incomplete insights into the disease process. For example, immune cells are thought to be responsible for a significant portion of muscle cell death in themdxmouse; however, the role and time course of the immune response in the dystrophic process have not been well described. In this paper we constructed a simple mathematical model to investigate the role of the immune response in muscle degeneration and subsequent regeneration in themdxmouse model of Duchenne muscular dystrophy. Our model suggests that the immune response contributes substantially to the muscle degeneration and regeneration processes. Furthermore, the analysis of the model predicts that the immune system response oscillates throughout the life of the mice, and the damaged fibers are never completely cleared.
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Barclay, Jack K., Coral L. Murrant, Nancy E. Woodley, and Stacey A. Reading. "Potential Interactions Among Vascular and Muscular Functional Compartments During Active Hyperemia." Canadian Journal of Applied Physiology 28, no. 5 (October 1, 2003): 737–53. http://dx.doi.org/10.1139/h03-056.
Повний текст джерелаАнотація:
The increase in blood flow that accompanies the start of contractions (active hyperemia) is a complex phenomenon involving a fast phase in which blood flow increases quickly and then slows or decreases (seek phase) before stabilizing at a flow corresponding to the metabolic rate (matched phase). This pattern of blood flow change involves contributions from a flow-induced increase in flow, a response to short periods of occlusion or partial occlusion due to force generated by the muscle contraction, and metabolism. Even denervated, the vascular bed, which consists of endothelial cells, vascular smooth muscle cells, and an adventitial layer that has significant secretory potential, is able to coordinate the response pattern. Within the vascular wall, communication is possible bidirectionally across the wall and also along the wall in a retrograde or upstream direction. The signals involved, which range from endothelial cell products such as nitric oxide and endothelin to adenosine, a skeletal muscle metabolite, appear to be situation- and time-dependent. In addition to the communication potential within and along the vascular wall, signals from the vascular system are able to exert inotropic effects on mammalian skeletal muscle. Key words: bidirectional signaling, postcontraction hyperemia, flow-induced flow changes, signal plasticity
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Vladimirov, Nikolay Mikhailovich. "MYOKINES, THEIR ROLE IN MUSCLE CONTRACTION." Scientific medical Bulletin of Ugra 27, no. 1 (2021): 4–11. http://dx.doi.org/10.25017/2306-1367-2021-27-1-4-11.
Повний текст джерелаАнотація:
Skeletal muscles are the largest organ in the human body, making up 40–50% of the total human body weight. This work is devoted to the study of physical activity on the athlete’s body. Given that the muscular system is more multifunctional than previously thought, and is able to aff ect many systems of the body through the synthesis and secretion of cytokines-classical regulators of the immune system, classifi ed as myokines. In this review article, we summarize our current knowledge of the main identifi ed and characterized myokines, focusing on their biological activity and functions. Through regular exercise, muscle-induced factors called myokines can exert and play an important role in protecting against many diseases.
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Valenzuela, Cristián A., Rodrigo Zuloaga, Luis Mercado, Ingibjörg Eir Einarsdottir, Björn Thrandur Björnsson, Juan Antonio Valdés, and Alfredo Molina. "Chronic stress inhibits growth and induces proteolytic mechanisms through two different nonoverlapping pathways in the skeletal muscle of a teleost fish." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 314, no. 1 (January 1, 2018): R102—R113. http://dx.doi.org/10.1152/ajpregu.00009.2017.
Повний текст джерелаАнотація:
Chronic stress detrimentally affects animal health and homeostasis, with somatic growth, and thus skeletal muscle, being particularly affected. A detailed understanding of the underlying endocrine and molecular mechanisms of how chronic stress affects skeletal muscle growth remains lacking. To address this issue, the present study assessed primary (plasma cortisol), secondary (key components of the GH/IGF system, muscular proteolytic pathways, and apoptosis), and tertiary (growth performance) stress responses in fine flounder ( Paralichthys adspersus) exposed to crowding chronic stress. Levels of plasma cortisol, glucocorticoid receptor 2 ( gr2), and its target genes ( klf15 and redd1) mRNA increased significantly only at 4 wk of crowding ( P < 0.05). The components of the GH/IGF system, including ligands, receptors, and their signaling pathways, were significantly downregulated at 7 wk of crowding ( P < 0.05). Interestingly, chronic stress upregulated the ubiquitin-proteasome pathway and the intrinsic apoptosis pathways at 4wk ( P < 0.01), whereas autophagy was only significantly activated at 7 wk ( P < 0.05), and meanwhile the ubiquitin-proteasome and the apoptosis pathways returned to control levels. Overall growth was inhibited in fish in the 7-wk chronic stress trial ( P < 0.05). In conclusion, chronic stress directly affects muscle growth and downregulates the GH/IGF system, an action through which muscular catabolic mechanisms are promoted by two different and nonoverlapping proteolytic pathways. These findings provide new information on molecular mechanisms involved in the negative effects that chronic stress has on muscle anabolic/catabolic signaling balance.
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Rudlof, Maximilian E., Boštjan Šimunić, Bianca Steuber, Till O. Bartel, Ruslan Neshev, Petra Mächler, Andreas Dorr, Rainer Picha, Karin Schmid-Zalaudek, and Nandu Goswami. "Effects of Meditation on Cardiovascular and Muscular Responses in Patients during Cardiac Rehabilitation: A Randomized Pilot Study." Journal of Clinical Medicine 11, no. 20 (October 18, 2022): 6143. http://dx.doi.org/10.3390/jcm11206143.
Повний текст джерелаАнотація:
Background: Cardiovascular diseases are the world’s number one cause of death, with exceeding psychosocial stress load being considered a major risk factor. A stress management technique that has repeatedly shown positive effects on the cardiovascular system is the Transcendental Meditation (TM) technique. The present pilot study aimed to investigate the potential effect of TM on the recovery of cardiac patients. Objectives: We hypothesized that practicing TM in patients undergoing a 4-week cardiac rehabilitation program augments the recovery of cardiovascular parameters and reduces skeletal muscle tone after rehabilitation. Methods: Twenty cardiac patients were recruited and randomly assigned to either the control or the TM group. Cardiovascular parameters were assessed with the Task Force Monitor (TFM) and skeletal muscle contractile properties by Tensiomyography during a sit-stand test, performed at the beginning and end of a 4-week in-patient rehabilitation program. Results: Systolic blood pressure (SBP) was significantly lower after 4 weeks of cardiac rehabilitation, while the RR-interval (RRI) significantly increased. At the skeletal muscle level, the contraction time and maximal displacement increased, though only in the gastrocnemius medialis and biceps femoris muscles and not in vastus lateralis. Group interactions were not observed for hemodynamic parameters nor for muscle contractile properties. Discussion: Although significant improvements in hemodynamic and muscular parameters were observed after 4 weeks of rehabilitation, we could not provide evidence that TM improved rehabilitation after 4 weeks. TM may unfold its effects on the cardiovascular system in the longer term. Hence, future studies should comprise a long-term follow-up.
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Kozhanova, T. V., S. S. Zhilina, T. I. Mescheryakova, M. Yu Shorina, I. F. Demenshin, G. G. Prokopiev, I. V. Kanivets, et al. "New mutation in the TRIP4 gene associated with congenital muscular dystrophy Davignon–Chauveau type (clinical case)." Neuromuscular Diseases 11, no. 3 (December 13, 2021): 51–63. http://dx.doi.org/10.17650/2222-8721-2021-11-3-51-63.
Повний текст джерелаАнотація:
Congenital muscular dystrophies are heterogeneous groups of neuromuscular diseases leading to hypotonia, progressive muscle weakness and dystrophic or structural signs in muscle biopsy. At the present time, 34 genes associated with congenital muscular dystrophy have been described. The clinical case of a rare form of congenital muscular dystrophia associated with a homozygous mutation in the TRIP4 gene in a patient with respiratory failure requiring respiratory support, neurological symptoms, muscular hypotonia, and multiple congenital malformations of skeletal system is presented for the first time in Russia. The undescribed pathogenic homozygous variant of the nucleotide sequence in the TRIP4 gene (chr15:64686179, c.136C>T, p.Arg46Ter, 2 exon, NM_016213.4) was detected by whole exome sequencing. The mutation in the TRIP4 gene was validated by Sanger sequencing in a child and its origin was investigated. The mother and father of the girl are carriers of the heterozygous variant in the TRIP4 gene. Identification of the genetic cause of a rare form of neuromuscular disease is important for determining the tactics of patient management and medical and genetic counseling of the family, as well as clarifying the pathogenesis of a rare pathology.