Готові списки джерел за темами / Skeletal muscular system

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Добірка наукової літератури з теми "Skeletal muscular system"

Автор: Grafiati
Опубліковано: 10 січня 2023
Оновлено: 28 січня 2023

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Статті в журналах з теми "Skeletal muscular system"

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.

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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.
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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.

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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.
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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.

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Анотація:
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.
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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.

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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.
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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.

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Анотація:
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.
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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.

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Анотація:
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.
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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.

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Анотація:
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.
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Більше джерел

Дисертації з теми "Skeletal muscular system"

1

Pattison, J. Scott. "Understanding muscle wasting through studies of gene expression and function." Free to MU Campus, others may purchase, 2004. http://wwwlib.umi.com/cr/mo/fullcit?p3164536.

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2

Wise, Andrew 1972. "Skeletal muscle : activation strategies, fatigue properties and role in proprioception." Monash University, Dept. of Physiology, 2001. http://arrow.monash.edu.au/hdl/1959.1/8355.

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3

Siles, Mena Laura. "Role of ZEB1 in skeletal muscle: Regulation of cell differentiation, response to tissue damage and regeneration." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/587110.

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ZEB1 is a transcription factor best known for its role in cancer progression and metastasis. It is also expressed during embryonic development of different tissues although its function and mechanism of action have not always been elucidated. In this dissertation I show that ZEB1 is involved in muscle differentiation during embryonic development and it is also required for muscle response after injury and regeneration. We found that, in the nucleus of myoblasts, ZEB1 represses muscle differentiation genes through direct binding to G/C-centered E-boxes present in the regulatory regions of muscle differentiation genes. Albeit to different degrees depending on the target gene, transcriptional repression of these genes by ZEB1 is mediated by its recruitment of the corepressor CtBP. Binding of ZEB1 to E-boxes in differentiation genes displaces MyoD and prevents their transcriptional activation during the myoblast stage. As myoblasts fuse, MyoD displaces ZEB1 from its DNA binding sites and differentiation proceeds. Knockdown of Zeb1 induces muscle differentiation genes, thus accelerating the formation of myotubes. Muscle regeneration after damage depends on a timely regulated transition from pro- to anti-inflammatory signals. Injury of Zeb1-deficient mice results in increased recruitment of inflammatory macrophages and expression of pro-inflammatory cytokines, which delays the regenerative process. Adult muscle regeneration relies on a pool of functional SCs and we show that Zeb1-deficient SCs undergo premature activation after isolation and culture by downregulating Pax7 and quiescence-associated genes (Foxo3, Hes genes) and upregulating Myod1. Moreover, its regenerative potential when transplanted into mdx hosts is reduced compared to wild-type SCs and exhibit increased senescence in culture. These results establish ZEB1 as an important potential regulator of muscle differentiation and regeneration by modulating inflammatory response and SC myogenic progression in response to injury. They also set ZEB1 as a potential therapeutic target in muscle dystrophies or following muscle insult.
ZEB1 és un factor de transcripció conegut pel seu paper en progressió tumoral i metàstasi. També s’expressa durant el desenvolupament embrionari de diferents teixits tot i que la seva funció i mecanisme d’acció encara no han estat establerts. En aquesta tesi mostro que ZEB1 està implicat en la diferenciació muscular durant el desenvolupament embrionari i que es necessari en la resposta al dany i regeneració muscular. Hem trobat que, en els nuclis dels mioblasts, ZEB1 reprimeix gens de diferenciació muscular per unió directa a seqüències “E-box” amb nucleòtids G/C en posició central en les seves regions reguladores. Encara que en diferents graus, depenent del gen diana, la repressió exercida per ZEB1 es fa mitjançant el reclutament del seu corepressor CtBP. La unió de ZEB1 a aquestes “E-boxes” desplaça MyoD evitant la seva activació transcripcional. Un cop els mioblasts es fusionen, MyoD desplaça ZEB1 de la seva unió a l’ADN donant lloc al procés de diferenciació. D’aquesta manera, la inhibició de Zeb1 indueix els gens de diferenciació muscular accelerant la formació de miotubs. La regeneració desprès del dany muscular depèn de la transició de senyals proinflamatoris a antiinflamatoris. La lesió muscular de ratolins deficients per Zeb1 produeix un elevat nombre de macròfags inflamatoris i l’expressió de citocines pro-inflamatories que retarden el procés regeneratiu. La regeneració del teixit muscular adult requereix la participació d’una població de cèl·lules satèl·lit funcionals. Els nostres resultats demostren que les cèl·lules satèl·lit deficients per Zeb1 s’activen precoçment un cop aïllades i posades en cultiu. Aquesta activació succeeix per la inhibició de Pax7 i de gens associats a la quiescència d’aquestes cèl·lules (Foxo3, Hes) i la activació de Myod1. A més a més, presenten una més alta senescència i la seva capacitat regenerativa és reduïda quan es trasplanten en ratolins mdx en comparació a les wild-type. Aquests resultats situen ZEB1 com un important regulador de la diferenciació i la regeneració muscular per modulació de la resposta inflamatòria i de la progressió de les cèl·lules satèl·lit en la resposta al dany muscular. També suggereixen ZEB1 com una potencial diana terapèutica en distròfies musculars o en resposta a la lesió del múscul esquelètic.
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Fernandes, Rui Manuel Pinhão. "Perturbações músculo-esqueléticas na região lombar da coluna-estudo comparativo entre nadadores de lazer e nadadores de competição." Master's thesis, Instituições portuguesas -- UTL-Universidade Técnica de Lisboa -- -Faculdade de Motricidade Humana, 1999. http://dited.bn.pt:80/29194.

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5

Costa, Manuel da Cunha. "Crioterapia-efeitos na homeostasia muscular após o exercício." Phd thesis, Instituições portuguesas -- UP-Universidade do Porto -- -Faculdade de Ciências do Desporto e de Educação Física, 2002. http://dited.bn.pt:80/29515.

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6

Acharyya, Swarnali. "Elucidating molecular mechanisms of muscle wasting in chronic diseases." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1180096565.

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7

Cruz, Adriana Sarmento de Oliveira. "Efeito do treinamento físico na modulação autonômica cardiovascular e no tecido muscular esquelético em pacientes com cardiopatia chagásica e função sistólica preservada." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-29112017-080615/.

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Introdução: Pacientes com cardiopatia chagásica têm hiperatividade do sistema nervoso simpático, piorando o prognóstico destes pacientes. Estão bem estabelecidos os benefícios do treinamento físico aeróbico (TF) no controle autonômico cardiovascular e na musculatura esquelética de pacientes com cardiopatia e disfunção ventricular. A hipótese da tese seria que o TF melhorasse a função autonômica cardiovascular e a estrutura e metabolismo muscular de pacientes com cardiopatia chagásica crônica (CCC) mesmo com função sistólica preservada, tendo em vista que parte destes pacientes evolui para a forma dilatada com disfunção ventricular e suas graves consequências. Objetivo: Avaliar o efeito do TF no controle autonômico cardiovascular e no tecido muscular esquelético em pacientes com CCC e função sistólica preservada. Métodos: Foram incluídos pacientes com duas reações sorológicas positivas para a doença de Chagas, alterações eletrocardiográficas, fração de ejeção do ventrículo esquerdo >= 55% e idade entre 30 e 60 anos. Vinte e quatro pacientes foram submetidos à primeira série de avaliações e foram randomizados em dois grupos: doze pacientes com CCC e função ventricular sistólica preservada submetidos ao TF além do seguimento clínico (ChT) e doze pacientes com CCC e função ventricular sistólica preservada não submetidos ao TF, apenas ao seguimento clínico (ChNT). Após quatro meses, oito pacientes finalizaram o protocolo de treinamento físico (ChT, n=08) e dez pacientes finalizaram o seguimento clínico (ChNT, n=10). A atividade nervosa simpática muscular (ANSM) foi avaliada pela técnica de microneurografia e o fluxo sanguíneo muscular (FSM) pela técnica de pletismografia de oclusão venosa. Variabilidade da frequência cardíaca e da pressão arterial foram analisadas utilizando sinais da frequência cardíaca captadas pelo eletrocardiograma e sinais da pressão arterial captados pelo finometer. A sensibilidade barorreflexa cardíaca foi avaliada com infusão de drogas vasotivas. A capacidade funcional foi avaliada pelo teste cardiopulmonar. A biópsia do músculo vasto-lateral foi realizada para as análises histológicas das fibras musculares e para avaliação da expressão gênica de Atrogin-1 e MuRF-1. O programa de TF foi realizado durante quatro meses, constando de 3 sessões semanais supervisionadas com duração aproximada de 60 minutos. Resultados: Como marcadores de TF, houve redução da frequência cardíaca de repouso e aumento do consumo de oxigênio pico. O TF diminuiu a hiperatividade simpática, colaborando para o aumento do FSM. O treinamento físico reduziu tanto a ANSM, quanto a atividade simpática cardíaca e vasomotora, e melhorou a sensibilidade barorreflexa cardíaca. A redução da ANSM esteve associada a redução da hiperatividade cardiovascular, melhora da sensibilidade barorreflexa cardíaca e redução da expressão gênica de Atrogin-1 e MuRF-1. Após período de quatro meses, o grupo ChT apresentou menor expressão gênica de Atrogin-1 em relação ao grupo ChNT. Conclusão: O TF provocou expressiva melhora na disfunção autonômica, no FSM e na capacidade funcional de pacientes com CCC e função sistólica preservada. Adicionalmente, a redução da ANSM esteve associada a melhora da sensibilidade barorreflexa cardíaca, redução do tônus simpático cardiovascular e redução da expressão gênica de Atrogin-1 e MuRF-1, genes envolvidos na atrofia muscular
[thesis]. São Paulo: Faculdade de Medicina, Universidade de São Paulo; 2017. Background: Patients with chagasic cardiomyopathy have sympathetic nervous system hyperactivity, worsening the prognosis of these patients. The benefits of aerobic training (ET) in cardiovascular autonomic control and skeletal muscle of heart failure patients are well established. The thesis hypothesis was that ET improves cardiovascular autonomic function and structure and metabolism muscle in chronic chagasic cardiopathy (CCC) patients even though preserved systolic function, considering that part of these patients develop the dilated form with ventricular dysfunction and its serious consequences. Objectives: To evaluate the effects of ET on cardiovascular autonomic control and skeletal muscle tissue in CCC patients and preserved systolic function. Methods: Patients with two positive serological reactions for Chagas disease, electrocardiographic alterations, left ventricular ejection fraction >= 55% and age between 30 and 60 years were included. Twenty-four patients underwent the first stage of evaluations and were randomized into two groups: Twelve CCC patients and preserved systolic ventricular function submitted to ET in addition to clinical follow-up (ET group) and twelve CCC patients and preserved systolic ventricular function submitted to only clinical follow-up not submitted to ET (NoET group). After four months, eight patients completed the ET protocol (ET, n = 08) and ten patients completed clinical follow-up (NoET, n = 10). Muscular sympathetic nerve activity (MSNA) was measured using microneurography technique and muscle blood flow (MBF) by the venous occlusion plethysmography technique. Heart rate and blood pressure variability were analyzed using heart rate signals captured by the electrocardiogram and blood pressure signals captured by the finometer. Cardiac baroreflex sensitivity was evaluated by infusion of vasoactive drugs. Functional capacity was determined by cardiopulmonary exercise test. Vastus lateralis muscle biopsy was performed for the histological analysis of muscle fibers and for the Atrogin-1 and MuRF-1 gene expression evaluation. ET program consisted of three 60-minute exercise sessions per week for four months. Results: As ET markers, there was a reduction in resting heart rate and an increase in peak oxygen consumption. ET reduced the sympathetic hyperactivity, contributing to the increase of the MBF. ET reduced both MSNA, as well as cardiac and vasomotor sympathetic activity, and improved cardiac baroreflex sensitivity. Reduction of MSNA was associated with a reduction in cardiovascular hyperactivity, improved cardiac baroreflex sensitivity, and reduced Atrogin-1 and MuRF-1 gene expression. After the four-month period, the ET group presented lower Atrogin-1 gene expression than the NoET group. Conclusion: ET improved significantly autonomic dysfunction, MBF and functional capacity of CCC patients and preserved systolic function. In addition, the reduction of ANSM was associated with improved cardiac baroreflex sensitivity, reduced sympathetic cardiovascular tone, and reduced Atrogin-1 and MuRF-1 gene expression, genes involved in muscle atrophy
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Sishi, Balindiwe J. N. "An investigation into the P13-K/AKT signalling pathway in TNF-a-induced muscle proeolysis in L6 myotubes." Thesis, Stellenbosch : Stellenbosch University, 2008. http://hdl.handle.net/10019.1/3039.

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Анотація:
Thesis (MSc (Physiological Sciences))--Stellenbosch University, 2008.
Introduction: Skeletal muscle atrophy is a mitigating complication that is characterized by a reduction in muscle fibre cross-sectional area as well as protein content, reduced force, elevated fatigability and insulin resistance. It seems to be a highly ordered and regulated process and signs of this condition are often seen in inflammatory conditions such as cancer, AIDS, diabetes and chronic heart failure (CHF). It has long been understood that an imbalance between protein degradation (increase) and protein synthesis (decrease) both contribute to the overall loss of muscle protein. Although the triggers that cause atrophy are different, the loss of muscle mass in each case involves a common phenomenon that induces muscle proteolysis. It is becoming evident that interactions among known proteolytic systems (ubiquitin-proteosome) are actively involved in muscle proteolysis during atrophy. Factors such as TNF-α and ROS are elevated in a wide variety of chronic inflammatory diseases in which skeletal muscle proteolysis presents a lethal threat. There is an increasing body of evidence that implies TNF-α may play a critical role in skeletal muscle atrophy in a number of clinical settings but the mechanisms mediating its effects are not completely understood. It is also now apparent that the transcription factor NF-κB is a key intracellular signal transducer in muscle catabolic conditions. This study investigated the various proposed signalling pathways that are modulated by increasing levels of TNF-α in a skeletal muscle cell line, in order to synthesize our current understanding of the molecular regulation of muscle atrophy. Materials and Methods: L6 (rat skeletal muscle) cells were cultured under standard conditions where after reaching ± 60-65% confluency levels, differentiation was induced for a maximum of 8 days. During the last 2 days, myotubes were incubated with increasing concentrations of recombinant TNF-α (1, 3, 6 and 10 ng/ml) for a period of 40 minutes, 24 and 48 hours. The effects of TNF-α on proliferation and cell viability were measured by MTT assay and Trypan Blue exclusion technique. Morphological assessment of cell death was conducted using the Hoechst 33342 and Propidium Iodide staining method. Detection of apoptosis was assessed by DNA isolation and fragmentation assay. The HE stain was used for the measurement of cell size. In order to determine the source and amount of ROS production, MitoTracker Red CM-H2 X ROS was utilised. Ubiquitin expression was assessed by immunohistochemistry. PI3-K activity was calculated by using an ELISA assay and the expression of signalling proteins was analysed by Western Blotting using phospho-specific and total antibodies. Additionally, the antioxidant Oxiprovin was used to investigate the quantity of ROS production in TNF-α-induced muscle atrophy. Results and Discussion: Incubation of L6 myotubes with increasing concentrations of recombinant TNF-α revealed that the lower concentrations of TNF-α used were not toxic to the cells but data analysis of cell death showed that 10 ng/ml TNF-α induced apoptosis and necrosis. Long-term treatment with TNF-α resulted in an increase in the upregulation of TNF- α receptors, specifically TNF-R1. The transcription factors NF-κB and FKHR were rapidly activated thus resulting in the induction of the ubiquitin-proteosome pathway. Activation of this pathway produced significant increases in the expression of E3 ubiquitin ligases MuRF-1 and MAFbx. Muscle fibre diameter appeared to have decreased with increasing TNF-α concentrations in part due to the suppressed activity of the PI3-K/Akt pathway as well as significant reductions in differentiation markers. Western blot analysis also showed that certain MAPKs are activated in response to TNF-α. No profound changes were observed with ROS production. Finally, the use Oxiprovin significantly lowered cell viability and ROS production. These findings suggest that TNF-α may elicit strong catabolic effects on L6 myotubes in a dose and time dependent manner. Conclusion: These observations suggest that TNF-α might have beneficial effects in skeletal muscle in certain circumstances. This beneficial effect however is limited by several aspects which include the concentration of TNF-α, cell type, time of exposure, culture conditions, state of the cell (disturbed or normal) and the cells stage of differentiation. The effect of TNF-α can be positive or negative depending on the concentration and time points analysed. This action is mediated by various signal transduction pathways that are thought to cooperate with each other. More understanding of these pathways as well as their subsequent upstream and downstream constituents is obligatory to clarify the central mechanism/s that control physiological and pathophysiological effects of TNF-α in skeletal muscle.
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Santos, Marcelo Rodrigues dos. "Efeito do treinamento físico isolado ou associado à reposição de testosterona em pacientes com insuficiência cardíaca." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-17012014-122243/.

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Introdução. A insuficiência cardíaca (IC) é caracterizada por exacerbação da atividade nervosa simpática muscular (ANSM), baixa tolerância ao esforço e dispneia. Além disso, é característico nessa população o desequilíbrio entre o anabolismo e catabolismo, favorecendo dessa maneira uma acentuada perda da massa magra muscular, o que agrava ainda mais a qualidade de vida nos pacientes com IC. Dentre as alterações anabólicas observadas na IC avançada destaca-se a diminuição dos hormônios GH, IGF-1 e testosterona. A testosterona, um importante hormônio para as características masculinizantes e na manutenção da massa muscular, apresenta acentuada redução com o avançar da doença. Esta perda da massa magra, leva ao processo de caquexia muscular e consequente atrofia, com diminuição da força e da capacidade funcional do paciente com IC. A reposição de testosterona nesses pacientes tem sido estudada e se mostra uma importante terapêutica para melhorar a capacidade funcional e força muscular. Porém, não se conhece claramente o papel deste tratamento medicamentoso sobre o processo anabólico muscular, bem como na melhora da composição corporal. O exercício físico como tratamento não medicamentoso tem sido amplamente recomendado na IC por reduzir a ANSM, melhorar o fluxo sanguíneo periférico, aumentar a força muscular e melhorar a qualidade de vida. Entretanto, a combinação das estratégias do exercício físico associado à terapia de reposição de testosterona, não é conhecido em pacientes com IC. Métodos. 24 pacientes com IC foram randomizados em 3 grupos: Treinamento (TR, n=9), Testosterona (T, n=8) e Treino+Testosterona (TRT, n=7). A ANSM foi avaliada pela técnica de Microneurografia. O fluxo sanguíneo do antebraço foi avaliado pela pletismografia de oclusão venosa. A composição corporal foi avaliada pela densitometria (DEXA). A biópsia do músculo vasto-lateral foi feita para avaliarmos a área de secção transversa da fibra e a tipagem de fibras musculares. A qualidade de vida foi avaliada pelo questionário de Minnesota. O treinamento físico aeróbio em bicicleta foi realizado 3 vezes por semana, com 40 minutos de exercício por sessão, pelo período de 4 meses. A reposição de testosterona foi realizada pela administração intramuscular de undecilato de testosterona pelo período de 4 meses. Resultados. Após 4 meses de intervenção, observamos restauração dos níveis de testosterona em todos os grupos. A ANSM reduziu nos grupos TR e TRT. Não houve aumento do fluxo sanguíneo entre os grupos. O consumo de oxigênio aumentou em todos os grupos, porém apenas o grupo TRT aumentou a potência máxima ao exercício. A massa magra apresentou aumento significativo apenas no grupo TRT. Não observamos mudança no conteúdo mineral ósseo entre os grupos. Apenas o grupo TRT aumentou de maneira significativa a área de secção transversa das fibras tipo I (oxidativas). A qualidade de vida melhorou apenas nos grupos TR e TRT. Conclusões. O exercício físico associado à terapia de reposição de testosterona se mostrou mais eficaz em reduzir a ANSM, aumentar a capacidade funcional, a força muscular, a massa magra com um importante aumento das fibras do tipo I. Nossos resultados enfatizam a importância do exercício físico em pacientes com IC e traz uma nova perspectiva com a associação da testosterona para pacientes com hipogonadismo
Introduction. Heart failure (HF) is characterized by exacerbation of muscle sympathetic nerve activity (MSNA), exercise intolerance and dyspnea. Furthermore, is characteristic in this population the imbalance between anabolism and catabolism which lead to loss of skeletal muscle mass worsening quality of life in HF patients. Prior studies have demonstrated decrease in anabolic hormones such as GH, IGF-1 and testosterone. Testosterone, an important hormone for masculinization feature and maintenance of muscle mass, shows sharp decline in advanced HF. Loss muscle mass leads to cachexia and atrophy which decrease strength and functional capacity in HF patients. Testosterone replacement in these patients has been studied and shows an important therapeutic to enhance functional capacity and muscle strength. However it is not known the role of this medical treatment on muscle anabolic process as well as on body composition. Physical exercise as a non-medication treatment has been widely recommended to reduce MSNA, enhance peripheral blood flow, increase muscle strength and improve quality of life. However, the combination of the strategies of physical exercise associated with testosterone replacement therapy is not known in HF patients. Methods. 24 HF patients were randomized in 3 groups: Training (TR, n=9), Testosterone (T, n=8) and Training+Testosterone (TRT, n=7). MSNA was recorded by microneurography technic. Forearm blood flow was evaluated by venous occlusion plethysmography. Body composition was measured by densitometry (DEXA). Muscle biopsy was done in vastus lateralis to evaluate the cross-sectional area and type of fibers. Quality of life was assessed by Minnesota living with heart failure questionnaire. Aerobic exercise training on a bicycle was performed 3 times per week, with 40 minutes of exercise per session, for a period of 4 months. Testosterone replacement was performed by intramuscular administration of testosterone undecylate for a period of 4 months. Results. After 4 months testosterone levels were restored in all groups. MSNA decreased in TR and TRT groups. There was no increase in blood flow between groups. Oxygen consumption increased in all groups, but only the TRT group showed increase in maximum power to exercise. Lean body mass increased significantly only in the TRT group. We did not observe changes in bone mineral content between groups. Only TRT group significantly increased the cross-sectional area of type I fibers (oxidative). The quality of life improved only in TR and TRT groups. Conclusions. Exercise training associated with testosterone replacement therapy was more effective in reducing MSNA, increase functional capacity, muscle strength, lean mass with a significant increase in type I fibers. Our results emphasize the importance of physical exercise in patients with HF and bring a new perspective to association testosterone for patients with hypogonadism
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Corrêa, Lígia de Moraes Antunes. "Efeito do treinamento físico no controle mecanorreflexo e metaborreflexo da atividade nervosa simpática muscular em pacientes com insuficiência cardíaca." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-09092013-153651/.

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Introdução. A hiperativação nervosa simpática é característica marcante da insuficiência cardíaca. Estudos apontam alterações no controle ergorreflexo muscular (mecano e metaborreflexo) como mecanismos potenciais para explicar esta modificação autonômica. Os mecanorreceptores (fibras do grupo III), que são ativadas pelo aumento no tônus muscular e modulados por metabólitos da via das ciclooxigenases, encontram-se hipersensibilizadas na insuficiência cardíaca. Ao contrário, a sensibilidade dos metaborreceptores (fibras do grupo IV), que são ativados pelo acúmulo de metabólitos durante as contrações musculares e modulados pelos receptores TRPV1 e CB1, encontra-se diminuída na insuficiência cardíaca. Por outro lado, o treinamento físico tem se mostrado uma importante ferramenta no tratamento da insuficiência cardíaca. Ele reduz os níveis de atividade nervosa simpática muscular (ANSM) no repouso e durante o exercício em pacientes portadores desta síndrome. Dessa forma, neste estudo, nós testamos a hipótese de que o treinamento físico melhoraria o controle mecano e metaborreflexo da ANSM em pacientes com insuficiência cardíaca, e se essa melhora está associada às alterações na via das ciclooxigenases e na expressão dos receptores TRPV1 e CB1, respectivamente. Métodos. Pacientes com insuficiência cardíaca foram consecutivamente e aleatoriamente divididos em dois grupos: insuficiência cardíaca não treinado (ICNT, n=17) e insuficiência cardíaca treinado (ICT, n=17). A ANSM foi avaliada pela técnica de microneurografia e o fluxo sanguíneo muscular (FSM) pela pletismografia de oclusão venosa. A frequência cardíaca (FC) e a pressão arterial (PA) foram avaliadas por medida não invasiva a cada batimento (Finometer). Foi realizada biopsia muscular do vasto lateral para análise de expressão gênica. O treinamento físico aeróbio foi realizado em ciclo ergômetro, em intensidade moderada, por 40 minutos, três vezes por semana, durante 16 semanas. A sensibilidade mecanorreflexa foi calculada pelo delta absoluto entre o pico do exercício passivo, realizado na perna esquerda, e a média do registro basal. A sensibilidade metaborreflexa foi calculada pelo delta absoluto entre o 1º minuto de oclusão circulatória pós-exercício na perna esquerda e a média do registro basal. Resultados. O treinamento físico reduziu a ANSM e aumentou o FSM no repouso. O treinamento físico diminuiu significativamente as respostas de ANSM durante o exercício passivo no grupo ICT. As repostas de PA média também foram menores no grupo ICT quando comparado ao grupo ICNT. Não houve alterações significativas nas repostas de FC, PA sistólica, PA diastólica e FSM durante o exercício passivo no grupo ICT. Em relação à sensibilidade metaborreflexa, o treinamento físico aumentou expressivamente as respostas de ANSM no 1º minuto de oclusão circulatória no grupo ICT. As respostas de FC, PA e FSM não foram alteradas neste grupo. Não foram observadas alterações significativas nos controles mecano e metaborreflexo musculares no grupo ICNT. Além disso, o treinamento físico reduziu significativamente a expressão gênica da enzima COX-2 e do receptor EP4 e aumentou significativamente a expressão dos receptores TRPV1 e CB1 no grupo ICT. Não foram verificadas alterações significativas nas expressões gênicas do grupo ICNT. Conclusões. O treinamento físico normaliza os controles mecano e metaborreflexo da ANSM em pacientes com insuficiência cardíaca. Estas alterações podem estar associadas às alterações na expressão gênica da enzima COX-2 e receptor EP4, e dos receptores TRPV1 e CB1, respectivamente. Em conjunto, estes achados podem explicar, pelo menos em parte, a diminuição da atividade nervosa simpática e a melhora na tolerância aos esforços em pacientes com insuficiência cardíaca
Introduction. Sympathoexcitation is the hallmark of heart failure. Studies suggest changes in ergoreflex muscle control (mechanoreflex and metaboreflex) as potential mechanisms to explain this autonomic alteration in heart failure. Mechanoreceptors (group III fibers) that are activated by mechanical stimuli and modulated by cyclooxygenase pathway metabolites are hypersensitive in heart failure. In contrast, the sensitivity of metaboreceptors fibers (group IV) that are activated by increases in ischemic metabolites during muscle contractions and modulated by TRPV1 and CB1 receptors is blunted in heart failure. On the other hands, exercise training has been shown to be an important strategy in the treatment of heart failure. It reduces the levels of muscle sympathetic nerve activity (MSNA) at rest and during exercise in patients suffering of this syndrome. Thus, we tested the hypothesis that exercise training would improve the mechanoreflex and metaboreflex control of MSNA in heart failure patients. In addition, we investigated whether the improvement in the mechanoreflex and metaboreflex control is related to changes in the cyclooxygenase pathway and expression of TRPV1 and CB1 receptors, respectively. Methods. Patients with heart failure were consecutively and randomly divided into two groups: heart failure untrained (HFUT, n = 17) and heart failure exercise-trained (HFET, n = 17). MSNA was measured by microneurography technique and muscle blood flow (MBF) by venous occlusion plethysmography. Heart rate (HR) and blood pressure (BP) were assessed by noninvasive measure on a beat-to-beat basis (Finometer). Gene expression analysis was investigated by vastus lateralis muscle biopsy. Aerobic exercise training was performed on a cycle ergometer at moderate intensity, three 40-min session/wk for 16 weeks. Mechanoreflex sensitivity was evaluated by means the absolute difference in MSNA at peak passive exercise and baseline. Metaboreflex sensitivity was calculated by means the absolute difference in MSNA at 1st min after exercise period with muscle circulatory arrest and baseline. Results. Exercise training reduced MSNA and increased MBF. Exercise training significantly decreased MSNA responses during passive exercise. The mean BP response was lower in HFET group when compared to HFUT group. There were no significant changes in HR, systolic and diastolic BP and MBF responses during passive exercise in HFET group. Regarding metaboreflex sensitivity, exercise training significantly increased the MSNA responses at 1st minute of post exercise circulatory arrest. The responses of HR, BP and MBF were unchanged after exercise training. No significant changes were observed in mechanoreflex and metaboreflex control in the HFUT group. Furthermore, exercise training significantly reduced gene expression of COX-2 and EP4 receptor and significantly increased expression of TRPV1 and CB1 receptors. There were no significant changes in the gene expressions in the HFUT group. Conclusions. Exercise training improves mechanoreflex and metaboreflex control of MSNA in heart failure patients. These changes may be associated with changes in gene expression of COX-2 and EP4 receptor and TRPV1 and CB1 receptor, respectively. Together, these findings may explain, at least in part, the decrease in sympathetic nerve activity and the improvement in exercise tolerance in patients with heart failure
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Книги з теми "Skeletal muscular system"

1

Steve, Parker. Muscular and skeletal systems. Mankato, MN: New Forest Press, 2010.

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E, Riddle Janet T., Nicoll Kathleen B, and Rowantree Isabella I, eds. The skeletal system and the muscular system. Edinburgh: Churchill Livingstone, 1989.

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Movement: The muscular and skeletal system. New York: Dillon Press, 1993.

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The skeletal and muscular systems. New York: Chelsea House, 2009.

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Samuel, Hiti, and World Book Inc, eds. The skeletal and muscular systems. Chicago: World Book, a Scott Fetzer company, 2014.

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Caputo, Christine A. Bones and muscles: The skeletal and muscular system. New York: Scholastic, 2011.

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Johns, Deloris M. The skeletal and muscular systems: A laboratory manual. Dubuque, Iowa: Kendall/Hunt Pub. Co., 1996.

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Clark, Katie. A tour of your muscular and skeletal systems. North Mankato, Minn: Capstone Press, 2013.

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Bastian, Glenn F. An illustrated review of the skeletal and muscular systems. New York, NY: HarperCollins College Publishers, 1993.

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The muscular system manual: The skeletal muscles of the human body. 2nd ed. St. Louis, Mo: Elsevier Mosby, 2005.

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Частини книг з теми "Skeletal muscular system"

1

Schramm, Nicolai, Sabine Weckbach, Stephen Eustace, and Niamh M. Long. "Whole-Body MRI for Evaluation of the Entire Muscular System." In Magnetic Resonance Imaging of the Skeletal Musculature, 55–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/174_2013_873.

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Clément, Gilles. "The Musculo-Skeletal System in Space." In Fundamentals of Space Medicine, 181–216. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9905-4_5.

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Pelechas, Eleftherios, Evripidis Kaltsonoudis, Paraskevi V. Voulgari, and Alexandros A. Drosos. "Examination of the Musculoskeletal System." In Illustrated Handbook of Rheumatic and Musculo-Skeletal Diseases, 1–22. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-03664-5_1.

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Bird, Howard A. "The Voice and the Musculo-Skeletal System." In Performing Arts Medicine in Clinical Practice, 39–52. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-12427-8_4.

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Kherbache, Houda, Lahcene Bouabdellah, Mohamed Mokdad, Ali Hamaïdia, and Abdenacer Tezkratt. "Musculo Skeletal Disorders (MSDs) Among Algerian Nurses." In Advances in Intelligent Systems and Computing, 289–97. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-96098-2_38.

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Tanabe, Yuzo, Man Woo, and Ikuya Nonaka. "X Chromosome-Linked Muscular Dystrophy (mdx) of the Skeletal Muscle, Mouse." In Cardiovascular and Musculoskeletal Systems, 149–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76533-9_22.

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Mizuuchi, Ikuo, Yuto Nakanishi, Tomoaki Yoshikai, Masayuki Inaba, and Hirochika Inoue. "Body Information Acquisition System of Redundant Musculo-Skeletal Humanoid." In Springer Tracts in Advanced Robotics, 249–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/11552246_24.

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Ong, Hoo Dennis, Hooshang Hemami, and Sheldon Simon. "Simulation Studies of Musculo-Skeletal Dynamics in Cycling and Sitting on a Chair." In Multiple Muscle Systems, 518–33. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4613-9030-5_32.

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Cuadrado, Javier, Urbano Lugris, Francisco Mouzo, and Florian Michaud. "Musculo-skeletal Modeling and Analysis for Low-Cost Active Orthosis Customization and SCI Patient Adaptation." In IUTAM Symposium on Intelligent Multibody Systems – Dynamics, Control, Simulation, 41–54. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-00527-6_2.

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Marozzi, E., M. Caligara, C. Mecacci, and U. Genovese. "Comparison between Morphine Levels in the Blood and in the Musculo-Skeletal System of Subjects Who Died of Acute Intravenous Narcotism." In Acta Medicinæ Legalis Vol. XLIV 1994, 443–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79523-7_140.

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Тези доповідей конференцій з теми "Skeletal muscular system"

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Chen, Michael Z. Q., Kai Shen, and Chao Zhai. "A biomechanical model of human muscular-skeletal system with inertial effects." In 2016 35th Chinese Control Conference (CCC). IEEE, 2016. http://dx.doi.org/10.1109/chicc.2016.7554841.

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Hartl, Darren J., Gregory W. Reich, and Philip S. Beran. "Additive Topological Optimization of Muscular-Skeletal Structures via Genetic L-System Programming." In 24th AIAA/AHS Adaptive Structures Conference. Reston, Virginia: American Institute of Aeronautics and Astronautics, 2016. http://dx.doi.org/10.2514/6.2016-1569.

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Imamura, Takashi, Chisato Teraoka, Kazuhiko Terashima, and Zhong Zhang. "Muscular Power Estimation in a Tele-Rehabilitation System Using a Skeletal-Linkage Model." In 2006 SICE-ICASE International Joint Conference. IEEE, 2006. http://dx.doi.org/10.1109/sice.2006.315005.

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Koeppen, Ryan, Meghan E. Huber, Dagmar Sternad, and Neville Hogan. "Controlling Physical Interactions: Humans Do Not Minimize Muscle Effort." In ASME 2017 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dscc2017-5202.

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Physical interaction with tools is ubiquitous in functional activities of daily living. While tool use is considered a hallmark of human behavior, how humans control such physical interactions is still poorly understood. When humans perform a motor task, it is commonly suggested that the central nervous system coordinates the musculo-skeletal system to minimize muscle effort. In this paper, we tested if this notion holds true for motor tasks that involve physical interaction. Specifically, we investigated whether humans minimize muscle forces to control physical interaction with a circular kinematic constraint. Using a simplified arm model, we derived three predictions for how humans should behave if they were minimizing muscular effort to perform the task. First, we predicted that subjects would exert workless, radial forces on the constraint. Second, we predicted that the muscles would be deactivated when they could not contribute to work. Third, we predicted that when moving very slowly along the constraint, the pattern of muscle activity would not differ between clockwise (CW) and counterclockwise (CCW) motions. To test these predictions, we instructed human subjects to move a robot handle around a virtual, circular constraint at a constant tangential velocity. To reduce the effect of forces that might arise from incomplete compensation of neuro-musculo-skeletal dynamics, the target tangential speed was set to an extremely slow pace (∼1 revolution every 13.3 seconds). Ultimately, the results of human experiment did not support the predictions derived from our model of minimizing muscular effort. While subjects did exert workless forces, they did not deactivate muscles as predicted. Furthermore, muscle activation patterns differed between CW and CCW motions about the constraint. These findings demonstrate that minimizing muscle effort is not a significant factor in human performance of this constrained-motion task. Instead, the central nervous system likely prioritizes reducing other costs, such as computational effort, over muscle effort to control physical interactions.
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Selk Ghafari, Ali, Ali Meghdari, and Gholam Reza Vossoughi. "Modeling of Human Lower Extremity Musculo-Skeletal Structure Using Bond Graph Approach." In ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-41558.

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A vector bond graph approach for dynamic modeling of human musculo-skeletal system is addressed in this article. In the proposed model, human body is modeled as a ten-segment, nine degree of freedom, mechanical linkage, actuated by ten muscles in sagittal plane. The head, arm and torso (HAT) are modeled as a single rigid body. Interaction of the feet with the ground is modeled using a spring-damper unit placed under the sole of each foot. The path of each muscle is represented by a straight line. Each actuator is modeled as a three-element, Hill-type muscle in series with tendon. The governing equations of motion generated by the proposed method are equivalent to those developed with more traditional techniques. However the models can be more easily used in conjunction with control models of neuro-muscular function for the simulation of overall dynamic motor performance. In the proposed structure, segments can be easily added or removed. Such a model may have applications in clinical diagnosis and modeling of paraplegic patients during robotic-assisted walking.
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Koganezawa, Koichi, Hiroshi Inomata, and Toshiki Nakazawa. "Stiffness Control of Multi-DOF Joint by Passive/Active Parallel Actuation." In ASME 2005 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2005. http://dx.doi.org/10.1115/detc2005-84387.

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This paper deals with mechanical stiffness control of multi-DOF joint. It fundamentally mimics skeleto-muscular system of human articulation, in which at least two muscles cooperatively handle one DOF under their antagonistic action. In the first part of the paper one describes a novel actuator called ANLES (Actuator with Non-Linear Elastic System) that mimics a skeletal muscle in the sense of having a non-linear elasticity. Next one introduces a basic formula for controlling stiffness of the joint as well as its angles using multiple ANLESes. It follows the evaluation of the proposed formula by the simulation analysis. Three DOF joint manipulated by six or eight tendons that are individually controlled by the ANLES is evaluated with respect to the stiffness control. Based on the results of the simulation a new mechanism for the wrist joint having three DOF is proposed in the practical feasibility, in which only four ANLESes are used to control the stiffness of the wrist.
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Tigue, James A., Sonoma Harris, Chris Anjewierden, and Stephen A. Mascaro. "Validation of Fingertip Force and Finger Pose in the UART Finger and Bond Graph Tendon Model During Surface Contact." In ASME 2017 Dynamic Systems and Control Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dscc2017-5245.

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The intricate tendon system of the human muscular-skeletal system contributes to the human hand’s dexterity. A complex bond graph model of the index finger was developed to give insight into this system. Previous validation of this model by use of the ACT hand was difficult due to static joint friction. A new robotic testbed, Utah’s Anatomically-correct Robotic Testbed (UART) finger, has been developed to mitigate this friction. Static force and position experiments were conducted with the UART finger in contact with a surface and were compared to the bond graph model. The results suggest that the model is capable of simultaneously predicting static poses and fingertip force. The average predicted joint angle error was 2.9°. The average fingertip force magnitude error was 7.4%, and the average fingertip force direction error was 4.3°.
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Forshaw, Robert V., Nicholas W. Snow, Jared M. Wolff, Mansour Zenouzi, and Douglas E. Dow. "Electromyography (EMG) Controlled Assistive Rehabilitation System." In ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-40238.

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Electromyography (EMG) is a method for monitoring the electrical activity of skeletal muscles. The EMG signal is used to diagnose neuromuscular diseases and muscular injuries. EMG can also be utilized as an indicator of user intent for a muscle contraction for a specific motion. This input signal could be used to control powered exoskeleton prostheses. Limbs with impaired motor function tend to have increased disuse that may result in further muscle weakness. Therapy and other physical activities that increase the use of an impaired limb may contribute to some recovery of motor function. A device that helps to perform activities of daily living may increase usage and enhance recovery. The objective of this project is to make developments toward an EMG controlled assistive rehabilitation system that monitors EMG signals of the bicep and triceps muscles, and drives a motor to assist with arm motion. A motor is used to develop torque that would assist rotations of the arm about the elbow. A pair of EMG sensors (one pair near the biceps and the other near the triceps muscle) transmits electrical activity of the arm to a microcontroller (Raspberry Pi, Raspberry Pi Foundation, United Kingdom). For the prototype, the EMG signal is sampled and rectified within a moving time window to determine the root mean squared (VRMS) value. This value is used by the microcontroller to generate a pulse-width modulated (PWM) signal that controls the motor. Sensors for the motor provide information to an algorithm on the microcontroller. The generated PWM signal is based on the Vrms values for the EMG signal. Testing and analysis has shown a correlation between the EMG Vrms amplitude and muscle generated torque. The EMG controlled assistive rehabilitation system shows promise for assisting motor function for rotations about the elbow. Further algorithmic development is needed to determine the appropriate amount of assistance from the motor for the motor function indicated by user intent.
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Chen, Kai, and Richard Foulds. "Optimization of Stiffness and Damping in Modeling of Voluntary Elbow Flexions." In ASME 2011 International Mechanical Engineering Congress and Exposition. ASMEDC, 2011. http://dx.doi.org/10.1115/imece2011-62219.

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A subsequent study of obstructed voluntary arm movement extended the relative damping concept, and incorporated the influential factors of the mechanical behavior of the neural, muscular and skeletal system in the control and coordination of arm posture and movement. A significant problem of the study is how this information should be used to modify control signals to achieve desired performance. This study used an Equilibrium Point Hypothesis (EPH) model to examine changes of controlling signals for arm movements in the context of adding perturbation/load in the form of forces/torques. The mechanical properties and reflex actions of muscles of the elbow joint were examined. Brief unexpected torque/force pulses of identical magnitude and time duration were introduced at different stages of the movement in a random order by a pre-programmed 3 degree of freedom (DOF) robotic arm (MOOG FCS HapticMaster). Key to this research is the optimization of B and K for each subject based on their HM only experimental data. The results shown in each of sections confirm that those parameters. Along with an EMG determined VT can be used successfully to model the perturbed trials. The results also show that the subjects may maintain the same control parameters (virtual trajectory, stiffness and damping) regardless of added perturbations that cause substantial changes in EMG activity and kinematics.
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10

Jones, Naveen, Manju Manuel, and Sreelal Pillai. "An embedded musculo-skeletal injury detection system." In 2016 International Conference on Emerging Technological Trends (ICETT). IEEE, 2016. http://dx.doi.org/10.1109/icett.2016.7873773.

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