994 resultados para Artificial muscle
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Neal, M., Meta-stable memory in an artificial immune network, Proceedings of the 2nd International Conference on Artificial Immune Systems {ICARIS}, Springer, 168-180, 2003,LNCS 2787/2003
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Timmis J Neal M J and Hunt J. Augmenting an artificial immune network using ordering, self-recognition and histo-compatibility operators. In Proceedings of IEEE international conference of systems, man and cybernetics, pages 3821-3826, San Diego, 1998. IEEE.
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Neal M J Timmis J and Hunt J. Data analysis with artificial immune systems, cluster analysis and kohonen networks: some comparisons. In Proceedings of IEEE international conference of systems, man and cybernetics, pages 922-927, Tokyo, 1999. IEEE.
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Timmis J and Neal M J. An artificial immune system for data analysis. In Proceedings of 3rd international workshop on information processing in cells and tissues (IPCAT), Indianapolis, U.S.A., 1999.
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Timmis J and Neal M J. A resource limited artificial immune system for data analysis. In Proceedings of ES2000 - Research and Development of Intelligent Systems, pages 19-32, Cambrige, U.K., 2000. Springer.
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Timmis J and Neal M J. Investigating the evolution and stability of a resource limited artificial immune system. In Proceedings of GECCO - special workshop on artificial immune systems, pages 40-41. AAAI press, 2000.
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Lacey, N. J., Lee, M. H. (2003). The Epistemological Foundations of Artificial Agents. Minds and Machines, 13, 339-365.
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Lee, M. H., Lacey, N. J. (2003). The Influence of Epistemology on the Design of Artificial Agents. Minds and Machines, 13 (3), 367-395
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RAE2008
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Sauze, C and Neal, M. 'Endocrine Inspired Modulation of Artificial Neural Networks for Mobile Robotics', Dynamics of Learning Behavior and Neuromodulation Workshop, European Conference on Artifical Life 2007, Lisbon, Portugal, September 10th-14th 2007.
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The intent of this review is to summarize current body of knowledge on the potential implication of the xanthine oxidase pathway (XO) on skeletal muscle damage. The possible involvement of the XO pathway in muscle damage is exemplified by the role of XO inhibitors (e.g., allopurinol) in attenuating muscle damage. Reliance on this pathway (as well as on the purine nucleotide cycle) could be exacerbated in conditions of low muscle glycogen availability. Thus, we also summarize current hypotheses on the etiology of both baseline and exertional muscle damage in McArdle disease, a condition caused by inherited deficiency of myophosphorylase. Because myophosphorylase catalyzes the first step of muscle glycogen breakdown, patients are unable to obtain energy from their muscle glycogen stores. Finally, we provide preliminary data from our laboratory on the potential implication of the XO pathway in the muscle damage that is commonly experienced by these patients.
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We recently generated a knock-in mouse model (PYGM p.R50X/p.R50X) of McArdle disease (myophosphorylase deficiency). One mechanistic approach to unveil the molecular alterations caused by myophosphorylase deficiency, which is arguably the paradigm of 'exercise intolerance', is to compare the skeletal-muscle tissue of McArdle, heterozygous, and healthy (wild type (wt)) mice. We analyzed in quadriceps muscle of p.R50X/p.R50X (n=4), p.R50X/wt (n=6) and wt/wt mice (n=5) (all male, 8 wk-old) molecular markers of energy-sensing pathways, oxidative phosphorylation (OXPHOS) and autophagy/proteasome systems, oxidative damage and sarcoplamic reticulum (SR) Ca handling. We found a significant group effect for total AMPK (tAMPK) and ratio of phosphorylated (pAMPK)/tAMPK (P=0.012 and 0.033), with higher mean values in p.R50X/p.R50X mice vs. the other two groups. The absence of massive accumulation of ubiquitinated proteins, autophagosomes or lysosomes in p.R50X/p.R50X mice suggested no major alterations in autophagy/proteasome systems. Citrate synthase activity was lower in p.R50X/p.R50X mice vs. the other two groups (P=0.036) but no statistical effect existed for respiratory chain complexes. We found higher levels of 4-hydroxy-2-nonenal-modified proteins in p.R50X/p.R50X and p.R50X/wt mice compared with the wt/wt group (P=0.011). Sarco(endo)plasmic reticulum ATPase 1 (SERCA1) levels detected at 110kDa tended to be higher in p.R50X/p.R50X and p.R50X/wt mice compared with wt/wt animals (P=0.076), but their enzyme activity was normal. We also found an accumulation of phosphorylated SERCA1 in p.R50X/p.R50X animals. Myophosphorylase deficiency causes alterations in sensory energetic pathways together with some evidence of oxidative damage and alterations in Ca handling but with no major alterations in OXPHOS capacity or autophagy/ubiquitination pathways, which suggests that the muscle tissue of patients is likely to adapt overall favorably to exercise training interventions.
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Burnley, M., Doust, J.H., Ball, D. and Jones, A.M. (2002) Effects of prior heavy exercise on VO2 kinetics during heavy exercise are related to changes in muscle activity. Journal of Applied Physiology 93, 167-174. RAE2008
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Infantolino, B., Gales, D., Winter, S., Challis, J., The validity of ultrasound estimation of muscle volumes, Journal of applied biomechanics, ISSN 1065-8483, Vol. 23, N?. 3, 2007 , pags. 213-217 RAE2008
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Robert Hasterok, Agnieszka Marasek, Iain S. Donnison, Ian Armstead, Ann Thomas, Ian P. King, Elzbieta Wolny, Dominika Idziak, John Draper and Glyn Jenkins (2006). Alignment of the genomes of brachypodium distachyon and temperate cereals and grasses using bacterial artificial chromosome landing with fluorescence in situ hybridization.Genetics, 73 (1), 349-362. Sponsorship: Royal Society / BBSRC;BBSRC RAE2008