20 resultados para Muscular tension

em CentAUR: Central Archive University of Reading - UK


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Kites offer considerable potential as wind speed sensors—a role distinct from their traditional use as instrument-carrying platforms. In the sensor role, wind speed is measured by kite-line tension. A kite tether line tension meter is described here, using strain gauges mounted on an aluminum ring in a Wheatstone bridge electronic circuit. It exhibits a linear response to tension 19.5 mV N−1 with good thermal stability mean drift of −0.18 N °C−1 over 5–45 °C temperature range and a rapid time response 0.2 s or better. Field comparisons of tether line tension for a Rokkaku kite with a fixed tower sonic anemometer show an approximately linear tension-wind speed relationship over the range 1–6 ms−1. © 2010 American Institute of Physics. doi:10.1063/1.3465560

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The excess surface energy of lamellae formed by an ABA triblock copolymer melt oriented parallel to a neutral surface is evaluated using self-consistent field theory (SCFT). Consistent with experiments and previous SCFT calculations, we find a preference for the A-rich domains at the surface, which can only be attributed to the architectural asymmetry between the A and B blocks. The behavior was previously attributed to a loss of bridging configurations that occurs when the B-domain resides at the surface. Here we demonstrate that it is actually the presence of chain ends that reduces the excess surface energy of an A-rich domain relative that of a B-rich domain.

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The cellular uptake of PMOs (phosphorodiamidate morpholino oligomers) can be enhanced by their conjugation to arginine-rich CPPs (cell-penetrating peptides). Here, we discuss our recent findings regarding (R-Ahx-R)(4)AhxB (Ahx is 6-aminohexanoic acid and B is beta-alanine) CPP-PMO conjugates in DMD (Duchenne muscular dystrophy) and murine coronavirus research. An (R-Ahx-R)(4)AhxB-PMO conjugate was the most effective compound in inducing the correction of mutant dystrophin transcripts in myoblasts derived from a canine model of DMD. Similarly, normal levels of dystrophin expression were restored in the diaphragms of mdx mice, with treatment starting at the neonatal stage, and protein was still detecTable 22 weeks after the last dose of an (R-Ahx-R)(4)AhxB-PMO conjugate. Effects of length, linkage and carbohydrate modification of this CPP on the delivery of a PMO were investigated in a coronavirus mouse model. An (R-Ahx-R)(4)AhxB-PMO conjugate effectively inhibited viral replication, in comparison with other peptides conjugated to the same PMO. Shortening the CPP length, modifying it with a mannosylated serine moiety or replacing it with the R(9)F(2) CPP significantly decreased the efficacy of the resulting PPMO (CPP-PMO conjugate). We attribute the success of this CPP to its stability in serum and its capacity to transport PMO to RNA targets in a manner superior to that of poly-arginine CPPs.

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In this paper we focused on the differences of mechanical properties of tension and normal wood of 1-year-old poplar trees, artificially tilted. Elastic and fracture properties have been measured and linked to the anatomy. Tension wood is well known because it prevents good surface finishing and leads to difficulties with sawing. We studied three main mechanical properties: young modulus, energy of cutting and longitudinal residual strain of maturation (with strain gauges) because of their importance in wood technology. Moreover, this work takes place in a larger project of study, the phenomena of axes re-orientation in trees (allowing by the production of reaction wood), where these data are required for biomechanical modelling. The results show that tension wood has a higher young modulus, needs a higher energy to be cut and exhibited a higher level of longitudinal residual strain of maturation than those of normal wood. The results suggest that these differences require deeper analysis of the wood than anatomy: measurement of microfibril orientation in the S2 layer and also the lignin composition in monomeric units.

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The mechanism of active stress generation in tension wood is still not fully understood. To characterize the functional interdependency between the G-layer and the secondary cell wall, nanostructural characterization and mechanical tests were performed on native tension wood tissues of poplar (Populus nigra x Populus deltoids) and on tissues in which the G-layer was removed by an enzymatic treatment. In addition to the well-known axial orientation of the cellulose fibrils in the G-layer, it was shown that the microfibril angle of the S2-layer was very large (about 36 degrees). The removal of the G-layer resulted in an axial extension and a tangential contraction of the tissues. The tensile stress-strain curves of native tension wood slices showed a jagged appearance after yield that could not be seen in the enzyme-treated samples. The behaviour of the native tissue was modelled by assuming that cells deform elastically up to a critical strain at which the G-layer slips, causing a drop in stress. The results suggest that tensile stresses in poplar are generated in the living plant by a lateral swelling of the G-layer which forces the surrounding secondary cell wall to contract in the axial direction.

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The aim of this study is to investigate flow-induced dynamic surface tension effects, similar to the well-known Marangoni phenomena, but solely generated by the nanoscale topography of the substrates. The flow-induced surface tension effects are examined on the basis of a sharp interface theory. It is demonstrated how nanoscale objects placed at the boundary of the flow domain result in the generation of substantial surface forces acting on the bulk flow.

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The major component of skeletal muscle is the myofibre. Genetic intervention inducing over-enlargement of myofibres beyond a certain threshold through acellular growth causes a reduction in the specific tension generating capacity of the muscle. However the physiological parameters of a genetic model that harbours reduced skeletal muscle mass have yet to be analysed. Genetic deletion of Meox2 in mice leads to reduced limb muscle size and causes some patterning defects. The loss of Meox2 is not embryonically lethal and a small percentage of animals survive to adulthood making it an excellent model with which to investigate how skeletal muscle responds to reductions in mass. In this study we have performed a detailed analysis of both late foetal and adult muscle development in the absence of Meox2. In the adult, we show that the loss of Meox2 results in smaller limb muscles that harbour reduced numbers of myofibres. However, these fibres are enlarged. These myofibres display a molecular and metabolic fibre type switch towards a more oxidative phenotype that is induced through abnormalities in foetal fibre formation. In spite of these changes, the muscle from Meox2 mutant mice is able to generate increased levels of specific tension compared to that of the wild type.

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Food restriction has a great impact on skeletal muscle mass by inducing muscle protein breakdown to provide substrates for energy production through gluconeogenesis. Genetic models of hyper-muscularity interfere with the normal balance between protein synthesis and breakdown which eventually results in extreme muscle growth. Mutations or deletions in the myostatin gene result in extreme muscle mass. Here we evaluated the impact of food restriction for a period of 5 weeks on skeletal muscle size (i.e., fibre cross-sectional area), fibre type composition and contractile properties (i.e., tetanic and specific force) in myostatin null mice. We found that this hyper-muscular model was more susceptible to catabolic processes than wild type mice. The mechanism of skeletal muscle mass loss was examined and our data shows that the myostatin null mice placed on a low calorie diet maintained the activity of molecules involved in protein synthesis and did not up-regulate the expression of genes pivotal in ubiquitin-mediated protein degradation. However, we did find an increase in the expression of genes associated with autophagy. Surprisingly, the reduction on muscle size was followed by improved tetanic and specific force in the null mice compared to wild type mice. These data provide evidence that food restriction may revert the hyper-muscular phenotype of the myostatin null mouse restoring muscle function.

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In this paper we use molecular dynamics to answer a classical question: how does the surface tension on a liquid/gas interface appear? After defining surface tension from the first principles and performing several consistency checks, we perform a dynamic experiment with a single simple liquid nanodroplet. At time zero, we remove all molecules of the interfacial layer of molecules, creating a fresh bare interface with the bulk arrangement of molecules. After that the system evolves towards equilibrium, and the expected surface tension is re-established. We found that the system relaxation consists of three distinct stages. First, the mechanical balance is quickly re-established. During this process the notion of surface tension is meaningless. In the second stage, the surface tension equilibrates, and the density profile broadens to a value which we call “intrinsic” interfacial width. During the third stage, the density profile continues to broaden due to capillary wave excitations, which does not however affect the surface tension.We have observed this scenario for monatomic Lennard-Jones (LJ) liquid as well as for binary LJ mixtures at different temperatures, monitoring a wide range of physical observables.

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Oculopharyngeal muscular dystrophy (OPMD) is an adult-onset disorder characterized by ptosis, dysphagia and proximal limb weakness. Autosomal-dominant OPMD is caused by a short (GCG)8–13 expansions within the first exon of the poly(A)-binding protein nuclear 1 gene (PABPN1), leading to an expanded polyalanine tract in the mutated protein. Expanded PABPN1 forms insoluble aggregates in the nuclei of skeletal muscle fibres. In order to gain insight into the different physiological processes affected in OPMD muscles, we have used a transgenic mouse model of OPMD (A17.1) and performed transcriptomic studies combined with a detailed phenotypic characterization of this model at three time points. The transcriptomic analysis revealed a massive gene deregulation in the A17.1 mice, among which we identified a significant deregulation of pathways associated with muscle atrophy. Using a mathematical model for progression, we have identified that one-third of the progressive genes were also associated with muscle atrophy. Functional and histological analysis of the skeletal muscle of this mouse model confirmed a severe and progressive muscular atrophy associated with a reduction in muscle strength. Moreover, muscle atrophy in the A17.1 mice was restricted to fast glycolytic fibres, containing a large number of intranuclear inclusions (INIs). The soleus muscle and, in particular, oxidative fibres were spared, even though they contained INIs albeit to a lesser degree. These results demonstrate a fibre-type specificity of muscle atrophy in this OPMD model. This study improves our understanding of the biological pathways modified in OPMD to identify potential biomarkers and new therapeutic targets.

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We have established the surface tension relaxation time in the liquid-solid interfaces of Lennard-Jones (LJ) liquids by means of direct measurements in molecular dynamics (MD) simulations. The main result is that the relaxation time is found to be almost independent of the molecular structures and viscosity of the liquids (at seventy-fold change) used in our study and lies in such a range that in slow hydrodynamic motion the interfaces are expected to be at equilibrium. The implications of our results for the modelling of dynamic wetting processes and interpretation of dynamic contact angle data are discussed.