Skeletal Muscle Atrophy
Mostrando 25-36 de 71 artigos, teses e dissertações.
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25. Processos adaptativos do tecido muscular esqueletico e tecido conjuntivo : repercussões sobre a flexibilidade
This study has as its objective to discuss the control mechanisms of structural adaptations in the connective and muscular tissues under different functional conditions. It consists in the development of the interpretations about the plasticity of the tissues related to physical activities in order to improve the motor system s flexibility. Therefore, this b
Publicado em: 1997
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26. Hsp27 inhibits IKKβ-induced NF-κB activity and skeletal muscle atrophy
Heat shock protein 25/27 (Hsp25/27) is a cytoprotective protein that is ubiquitously expressed in most cells, and is up-regulated in response to cellular stress. Previous work, in nonmuscle cells, has shown that Hsp27 inhibits TNF-α-induced NF-κB activation. During skeletal muscle disuse, Hsp25/27 levels are decreased and NF-κB activity increased, and thi
The Federation of American Societies for Experimental Biology.
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27. Plasminogen Activator Inhibitor Type 1 Up-Regulation Is Associated with Skeletal Muscle Atrophy and Associated Fibrosis
Muscle wasting remains a feature of many diseases and is counteracted by anabolic supplementation or exercise. Persisting atrophy-inducing conditions can be complicated by skeletal muscle fibrosis, which leads to functional impairment. Identification of early mechanisms that initiate atrophy-induced fibrosis may reveal novel targets for therapy or diagnosis.
American Society for Investigative Pathology.
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28. Nerve conduction studies, skeletal muscle EMG, and sphincter EMG in multiple system atrophy.
Although autonomic failure, parkinsonism, and cerebellar and pyramidal signs are well documented in multiple system atrophy, much less is known about the frequency and severity of involvement of the peripheral nervous system. The frequency and nature of peripheral nerve involvement has therefore been determined in 74 patients with multiple system atrophy usi
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29. Conditional Activation of Akt in Adult Skeletal Muscle Induces Rapid Hypertrophy
Skeletal muscle atrophy is a severe morbidity caused by a variety of conditions, including cachexia, cancer, AIDS, prolonged bedrest, and diabetes. One strategy in the treatment of atrophy is to induce the pathways normally leading to skeletal muscle hypertrophy. The pathways that are sufficient to induce hypertrophy in skeletal muscle have been the subject
American Society for Microbiology.
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30. Runx1 prevents wasting, myofibrillar disorganization, and autophagy of skeletal muscle
Disruptions in the use of skeletal muscle lead to muscle atrophy. After short periods of disuse, muscle atrophy is reversible, and even after prolonged periods of inactivity, myofiber degeneration is uncommon. The pathways that regulate atrophy, initiated either by peripheral nerve damage, immobilization, aging, catabolic steroids, or cancer cachexia, howeve
Cold Spring Harbor Laboratory Press.
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31. FoxO1 induces apoptosis in skeletal myotubes in a DNA-binding-dependent manner
Recent studies indicate that FoxO transcription factors play an important role in promoting muscle atrophy. To study mechanisms mediating effects of FoxO proteins on muscle wasting, FoxO1-estrogen receptor fusion proteins that are activated by treatment with 4-hydroxytamoxifen (4-OH-T) were stably transfected in C2C12 skeletal myoblasts using the pBABE retro
American Physiological Society.
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32. Inhibitors of prostaglandin synthesis or cathepsin B prevent muscle wasting due to sepsis in the rat.
Systemic infection with Streptococcus pneumoniae produced atrophy, decreased twitch and tetanic tension, and altered intracellular electrolyte composition in rat skeletal muscle. Cathepsin B activity was selectively elevated early in the course of illness. Luepeptin, a cathepsin B inhibitor, and indomethacin, a prostaglandin synthesis inhibitor, prevented mu
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33. Skeletal muscle dysfunction in chronic obstructive pulmonary disease
It has become increasingly recognized that skeletal muscle dysfunction is common in patients with chronic obstructive pulmonary disease (COPD). Muscle strength and endurance are decreased, whereas muscle fatigability is increased. There is a reduced proportion of type I fibers and an increase in type II fibers. Muscle atrophy occurs with a reduction in fiber
BioMed Central.
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34. Inhibitors of the proteasome reduce the accelerated proteolysis in atrophying rat skeletal muscles.
Several observations have suggested that the enhanced proteolysis and atrophy of skeletal muscle in various pathological states is due primarily to activation of the ubiquitin-proteasome pathway. To test this idea, we investigated whether peptide aldehyde inhibitors of the proteasome, N-acetyl-leucyl-leucyl-norleucinal (LLN), or the more potent CBZ-leucyl-le
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35. Specific changes in skeletal muscle myosin heavy chain composition in cardiac failure: differences compared with disuse atrophy as assessed on microbiopsies by high resolution electrophoresis.
OBJECTIVE: In congestive heart failure (CHF) the skeletal muscle of the lower limbs develops a myopathy with atrophy and shift from the slow type to the fast type fibres. The aim was to test the hypothesis that this myopathy is specific and not simply related to detraining, by comparing patients with different degrees of CHF with patients with severe muscle
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36. SLIMMER (FHL1B/KyoT3) Interacts with the Proapoptotic Protein Siva-1 (CD27BP) and Delays Skeletal Myoblast Apoptosis*
The fhl1 gene encoding four-and-a-half LIM protein-1 (FHL1) and its spliced isoform, SLIMMER, is mutated in reducing body myopathy, X-linked myopathy with postural muscle atrophy, scapuloperoneal myopathy, and rigid spine syndrome. In this study we have identified a novel function for SLIMMER in delaying skeletal muscle apoptosis via an interaction with the
American Society for Biochemistry and Molecular Biology.