Made available in DSpace on 2014-06-11T19:30:52Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-09-15Bitstream added on 2014-06-13T20:21:20Z : No. of bitstreams: 1 melo_sg_dr_rcla.pdf: 609577 bytes, checksum: a9d51fbcdf884c8d8bd0fca73bb98fef (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / A fadiga muscular é definida como a incapacidade que o músculo esquelético tem de gerar ou manter elevados níveis de força e potência muscular durante determinado tempo. Ela pode está associada a exercícios submáximos e/ou máximos, respondendo com diminuição da velocidade de contração das fibras musculares e aumento do tempo de relaxamento da musculatura trabalhada. Muitos estudos têm utilizado a eletromiografia de superfície (EMGs) para caracterizar a fadiga pelo aumento induzido da amplitude do sinal EMG, assim como investigar os mecanismos fisiológicos e biomecânicos associados ao processo de instalação da fadiga neuromuscular. O objetivo desse estudo foi analisar metodologias empregadas na determinação do limiar eletromiográfico na fadiga muscular (LFEMG), visando a comparação entre os métodos quanto a capacidade de determinar um índice de limiar anaeróbio eletromiográfico fidedigno. Participaram da pesquisa 10 jogadores amadores de futsal com médias de idade 20,8 anos, massa corpórea de 67,3kg e estatura de 1,75m. Executaram um protocolo incremental de corrida em esteira para análise do LFEMG. Foi utilizada a eletromiografia de superfície para músculos do membro inferior e coletados dados como amplitude do sinal e frequência mediana. Posteriormente os dados relativos à eletromiografia foram verificados quanto à normalidade (Shapiro-Wilk) e analisados (ANOVA) através do software SPSS. Os resultados confirmam a proposta de que o limiar de fadiga neuromuscular pode ser identificado por meio da análise do comportamento do sinal eletromiográfico durante o protocolo incremental de corrida, como observado em estudos anteriores, e que os métodos pesquisados não apresentam diferenças estatisticamente significativas entre eles, contudo necessitam-se padrões metodológicos mais confiáveis e reprodutíveis para determinação de índices de fadiga neuromuscular através da análise do sinal EMG / Muscle fatigue is defined as the inability the skeletal muscle has to generate or maintain high levels of muscle strength and power during a given time. It can submaximal exercise be associated with and / or maximum response with a decrease in speed of contraction of muscle fibers and increased time of relaxation of the muscles worked. Many studies have used surface electromyography (EMG) to characterize the fatigue induced by the increase of the amplitude of the EMG signal as well as investigate the physiological and biomechanical mechanisms associated with the installation process of neuromuscular fatigue. The aim of this study was to analyze the methodologies used in determining the electromyographic fatigue threshold (FTEMG) in order to compare the methods for their ability to determine an reliable index of anaerobic threshold electromyographic. 10 players of amateur soccer participated in the research with average age 20.8 years, body mass index of 67.3 kg and height 1.75 m. They performed an incremental protocol of treadmill running for FTEMG analysis. We used surface electromyography to lower limb muscles and collected as signal amplitude and median frequency. Subsequently, data were normalized relative to the electromyography (Shapiro-Wilk) analyzed (ANOVA) by SPSS software. The results confirm the proposal that the neuromuscular fatigue threshold can be identified by analyzing the behavior of electromyographic signals during incremental running protocol, as observed in previous studies, and that the methods surveyed have no statistically significant differences between them, however, more reliable and methodological standards for reproducible determination of indices of neuromuscular fatigue by EMG signal analysis are required

Tese de mestrado. Engenharia Biomédica. Faculdade de Engenharia. Universidade do Porto. 2007

No description available.

Abstract not available

Duchenne muscular dystrophy (DMD) and congenital muscular dystrophy 1A (MDC1A) are the two most common forms of muscular dystrophy in humans, caused by mutations in dystrophin and laminin α2 genes respectively. Both are severe forms of the disease that lead to premature death due and are both now known to have a significant effect on the central nervous system. This project investigated the role of both proteins involved in each of these diseases in cerebellar Purkinje cells of two murine models of disease: the mdx mouse a dystrophin-deficient model of DMD and the dy2J a laminin α2-deficient murine model of MDC1A. In the case of dystrophin further studies were undertaken in order to determine if increasing age had any effects on cerebellar function. It was found that there is no difference in electrophysiological characteristics (RMP, IR, eEPSP) of the cells when compared to appropriate control groups, nor was there any difference when young and aged dystrophin-deficient mdx groups were compared. Evoked IPSP characteristics were examined in young mdx cerebellar Purkinje cells and again no difference was found when compared to wildtype. There was a significant difference in response to the GABAA antagonist bicuculline, with wildtype increasing eEPSP amplitude by almost double that found in mdx. There was no difference in short term plasticity as measured by paired pulse facilitation in any of these groups. There was no difference in paired pulse depression at the inhibitory interneuron- Purkinje cell synapse of young wildtype and mdx cerebellar Purkinje cells. There a significant blunting of long term depression (LTD, (a form of long term synaptic plasticity) between young wildtype and mdx. When young wildtype animals were compared to aged wildtype animals LTD was found to be similar, when young mdx was compared to aged mdx, there was a recovery of LTD seen in the aged population. There was also significant differences in LTD found when littermate controls were compared to dy2J (laminin α2 mutants). A third of the phenotypic animals (dy2J) potentiated. Finally when rebound potentiation (a GABA-ergic form of long term synaptic plasticity in the cerebellum) was compared in young wildtype and mdx mice, mdx mice displayed depression, rather than the expected potentiation in contrast to potentiation (or no change) as seen in all wildtype cells.

Reprint. Thesis (Ph. D.)--Cornell University, 1913. / "Reprinted from the American Journal of Psychology, July, l9l3, vol. xxiv, pp. 305-359 ; October, 1913, vol. xxiv, pp. 508-519. Includes bibliographical references (p. 508-519).

Dissertation (MSc)--University of Stellenbosch, 2008. / Bibliography. Also available via the Internet.

Thesis (Ph. D.)--University of Chicago, Dept. of Molecular Genetics and Cell Biology, August 2003. / CD-ROM reproduces dissertation in PDF format; Adobe Acrobat required. Includes bibliographical references. Also available on the Internet.

No description available.

alpha- and beta-dystroglycan (DG) were first identified as members of an oligomeric, transmembrane complex expressed in muscle and linking laminin (LN) in the extracellular matrix (ECM) to dystrophin in the submembraneous cytoskeleton. This dystrophin-associated glycoprotein complex (DGC) has been proposed to perform a structural role in skeletal muscle, its loss leading to loss of membrane integrity, muscle fiber degeneration and muscular dystrophy. alpha- and beta-DG appear to form the core of the DGC since alpha-DG is a high affinity LN receptor while beta-DG is a transmembrane protein that anchors alpha-DG to the membrane and interacts with dystrophin intracellularly. In order to determine the involvement of DG in skeletal muscle homeostasis and in LN assembly, we generated mouse muscle cell lines deficient in DG expression. Extensive characterization of these cells revealed that DG is essential for LN assembly on the surface of mature myotubes but that it is not involved in the maintenance of membrane integrity in culture. However, DG-deficient cells show increased apoptotic cell death during and after the period of myoblast differentiation into myotubes, indicating that DG is important for muscle cell survival. / The ECM molecule agrin has been implicated in the induction of acetylcholine receptor (AChR) aggregation at the neuromuscular junction (NMJ). The C-terminus of agrin shares significant homology with the region of LN that interacts with alpha-DG; we therefore reasoned that alpha-DG could be an agrin receptor. Ligand overlay assays revealed that alpha-DG binds agrin with high affinity and antibody perturbation experiments indicated that alpha-DG is involved in agrin-induced aggregation of AChRs. The role of alpha-DG in AChR aggregation was further studied using the DG deficient muscle cell lines. We found that alpha-DG is involved in the later stages of agrin-induced AChR aggregation. / We further localized DG and two of its intracellular ligands, dystrophin and its autosomal homologue utrophin, to a synaptic layer in the retina suggesting a role for DG in central nervous system synapses. DG, utrophin and LN are also co-expressed around blood vessels indicating a possible function in blood-brain barrier homeostasis.