11 resultados para CRANIAL MUSCLES

em CentAUR: Central Archive University of Reading - UK


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Cranial sensory placodes are specialised areas of the head ectoderm of vertebrate embryos that contribute to the formation of the cranial sense organs and associated ganglia. Placodes are often considered a vertebrate innovation, and their evolution has been hypothesised as one key adaptation underlying the evolution of active predation by primitive vertebrates. Here, we review recent molecular evidence pertinent to understanding the evolutionary origin of placodes. The development of vertebrate placodes is regulated by numerous genes, including members of the Pax, Six, Eya, Fox, Phox, Neurogenin and Pou gene families. In the sea squirt Ciona intestinalis (a basal chordate and close relative of the vertebrates), orthologues of these genes are deployed in the development of the oral and atrial siphons, structures used for filter feeding by the sessile adult. Our interpretation of these findings is that vertebrate placodes and sea squirt siphon primordia have evolved from the same patches of specialised ectoderm present in the common ancestor of the chordates.

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Chemical compositions and physical properties of mixed-sex Thai indigenous (Gallus domesticus) and broiler (commercial breed, CP707) chicken biceps femoris and pectoralis muscles were determined. Indigenous chicken muscles contained higher protein contents but lower fat and ash contents compared to broiler muscles (P < 0.001). The amino acid profile of the indigenous chicken muscles was similar to that of the broiler muscles except they were slightly richer in glutamic acid (P < 0.05). The indigenous chicken muscles contained more saturated and less polyunsaturated fatty acids than the broiler muscles. There were no differences in the monounsaturated fatty acid contents between the breeds. The total collagen contents of indigenous pectoralis and biceps femoris muscles were 5.09 and 12.85 mg/g, respectively, which were higher than those found in broiler pectoralis (3.86 mg/g) and biceps femoris muscles (8.70 mg/g) (P < 0.001). Soluble collagen contents were lower for indigenous pectoralis and biceps femoris muscles, 22.16 vs. 31.38% and 26.06 vs. 33.87%, respectively. The CIE system values of lightness (L*), redness (a*), and yellowness (b*) of indigenous chicken muscles were higher than those of broiler muscles. The shear values of indigenous chicken muscles either raw or cooked were higher than those of broiler muscles (P < 0.05). After cooking, the shear values decreased for broiler biceps femoris and pectoralis muscles (P < 0.05), whereas no change was observed for indigenous chicken biceps femoris muscle (P > 0.05). Shear values increased for indigenous chicken pectoralis muscle (P < 0.05).

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The microstructure and thermal characteristics of Thai indigenous (Gallus domesticus) and broiler chicken (commercial line CP707) biceps femoris and pectoralis muscles were determined. Perimysium thicknesses were 14.2 mum for biceps femoris muscle and 7.10 mum for pectoralis muscle of indigenous chicken muscles, thicker than those of broiler muscles, which were 9.93 mum for biceps femoris muscle and 3.87 mum for pectoralis muscle (P < 0.05). Five endothermic peaks with peak transition temperatures (T-p) of 54.9, 61.7, 65.4, 70.6, and 76.1degreesC were obtained for broiler pectoralis muscle, whereas only 3 endothermic peaks (T-P of 56.6, 62.6, and 74.9degreesC were obtained for broiler biceps femoris muscle. Thai indigenous biceps femoris and pectoralis muscles had endothermic peaks with T-P ranges of 53.5 to 54.8, 60.7 to 61.9, and 75.9 to 76.9degreesC. The fiber diameters of Thai indigenous chicken muscles were greater (P < 0.05) than those of the broiler, 31.7 vs. 20.4 mum for biceps femoris muscle and 28.9 vs. 26.6 pm for pectoralis muscle, respectively. After cooking at 80degreesC for 10 min, the fiber diameter of indigenous chicken muscles significantly decreased while those of the broiler significantly increased. The mean of sarcomere lengths of the raw muscles ranged from 1.56 to 1.64 mun and decreased to 0.92 to 1.32 mum (P < 0.001) for broiler muscles and 1.22 to 1.35 mum (P < 0.001) for indigenous chicken muscles after cooking. The perimysium and endomysium of broiler muscles melted after cooking at 80degreesC, however, only slight disintegration was observed in these tissues in the indigenous chicken muscles.

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The spectral content of the myoelectric signals from the muscles of the remnant forearms of three persons with congenital absences (CA) of their forearms was compared with signals from their intact contra-lateral limbs, similar muscles in three persons with acquired losses (AL) and seven persons without absences [no loss (NL)]. The observed bandwidth for the CA subjects was broader with peak energy between 200 and 300 Hz. While the signals from the contra-lateral limbs and the AL and NL subjects was in the 100-150 Hz range: The mean skew of the signals from the AL subjects was 46.3 +/- 6.7 and those with NL of 45.4 +/- 8.7, while the signals from those with CAs had a skew of 11.0 +/- 11. The structure of the muscles of one CA subject was observed ultrasonically. The muscle showed greater disruption than normally developed muscles. It is speculated that the myographic signal reflects the structure of the muscle. which has developed in a more disorganized manner as a result of the muscle not being stretched by other muscles across the missing distal joint, even in the muscles that are used regularly to control arm prostheses.

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The aim of this paper is to show the feasibility of the use of functional electrical stimulation (FES) applied to the lower back muscles for pressure sores prevention in paraplegia. The hypothesis under study is that FES induces a change in the pressure distribution on the contact area during sitting. Tests were conducted on a paraplegic subject (T5), sitting on a standard wheelchair and cushion. Trunk extensors (mainly the erector spinae) were stimulated using surface electrodes placed on the skin. A pressure mapping system was used to measure the pressure on the sitting surface in four situations: (a) no stimulation; (b) stimulation on one side of the spine only; (c) stimulation on both sides, at different levels; and (d) stimulation at the same level on both sides, during pressure-relief manoeuvres. A session of prolonged stimulation was also conducted. The experimental results show that the stimulation of the erector spinae on one side of the spine can induce a trunk rotation on the sagittal plane, which causes a change in the pressure distribution. A decrease of pressure on the side opposite to the stimulation was recorded. The phenomenon is intensified when different levels of stimulation are applied to the two sides, and such change can be sustained for a considerable time (around 5 minutes). The stimulation did not induce changes during pressure-relief manoeuvres. Finally, from this research we can conclude that the stimulation of the trunk extensors can be a useful tool for pressure sores prevention, and can potentially be used in a routine for pressure sores prevention based on periodical weight shifts.

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In vertebrates, body musculature originates from somites, whereas head muscles originate from the cranial mesoderm. Neck muscles are located in the transition between these regions. We show that the chick occipital lateral plate mesoderm has myogenic capacity and gives rise to large muscles located in the neck and thorax. We present molecular and genetic evidence to show that these muscles not only have a unique origin, but additionally display a distinct temporal development, forming later than any other muscle group described to date. We further report that these muscles, found in the body of the animal, develop like head musculature rather than deploying the programme used by the trunk muscles. Using mouse genetics we reveal that these muscles are formed in trunk muscle mutants but are absent in head muscle mutants. In concordance with this conclusion, their connective tissue is neural crest in origin. Finally, we provide evidence that the mechanism by which these neck muscles develop is conserved in vertebrates.

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The recent celebrations of the centenary of the publication of the Futurist manifesto led to a renewed discussion of the ideas and artworks of the Italian artists’ group. Jacques Rancière related the Futurist ethos with the modernist project of liberating art from representation. Franco ‘Bifo’ Berardi, in his post-Futurist manifesto, also identified a historical irony at play in the emptying out of Futurism’s promise: a liberated mechanical humanity did indeed materialize, in a global economic system premised on financial servitude to the future via debt. However, these models continue to assess Futurism against an unchallenged humanism, finding it either supporting ideals of freedom and human rights despite itself, or else lacking in these areas. But Futurism is potentially more relevant than ever not in spite of its anti-humanist agenda, precisely because of it. Tom McCarthy annexes not Futurist art but Futurist writing to an emerging object oriented ontology that seeks to challenge the primacy of the human. If Futurism is to be repurposed as a critical concept, it can only do so by countering the humanist myth the liberal subject that underlies the current cultural and political hegemony of neo-liberalism.

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In vertebrates, body musculature originates from somites, whereas head muscles originate from the cranial mesoderm. Neck muscles are located in the transition between these regions. We show that the chick occipital lateral plate mesoderm has myogenic capacity and gives rise to large muscles located in the neck and thorax. We present molecular and genetic evidence to show that these muscles not only have a unique origin, but additionally display a distinct temporal development, forming later than any other muscle group described to date. We further report that these muscles, found in the body of the animal, develop like head musculature rather than deploying the programme used by the trunk muscles. Using mouse genetics we reveal that these muscles are formed in trunk muscle mutants but are absent in head muscle mutants. In concordance with this conclusion, their connective tissue is neural crest in origin. Finally, we provide evidence that the mechanism by which these neck muscles develop is conserved in vertebrates.

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Duchenne muscular dystrophy is a severe X-linked inherited muscle wasting disorder caused by mutations in the dystrophin gene. Adeno-associated virus (AAV) vectors have been extensively used to deliver genes efficiently for dystrophin expression in skeletal muscles. To overcome limited packaging capacity of AAV vectors (<5 kb), truncated recombinant microdystrophin genes with deletions of most of rod and carboxyl-terminal (CT) domains of dystrophin have been developed. We have previously shown the efficiency of mRNA sequence–optimized microdystrophin (ΔR4-23/ΔCT, called MD1) with deletion of spectrin-like repeat domain 4 to 23 and CT domain in ameliorating the pathology of dystrophic mdx mice. However, the CT domain of dystrophin is thought to recruit part of the dystrophin-associated protein complex, which acts as a mediator of signalling between extracellular matrix and cytoskeleton in muscle fibers. In this study, we extended the ΔR4-23/ΔCT microdystrophin by incorporating helix 1 of the coiled-coil motif in the CT domain of dystrophin (MD2), which contains the α1-syntrophin and α-dystrobrevin binding sites. Intramuscular injection of AAV2/9 expressing CT domain–extended microdystrophin showed efficient dystrophin expression in tibialis anterior muscles of mdx mice. The presence of the CT domain of dystrophin in MD2 increased the recruitment of α1-syntrophin and α-dystrobrevin at the sarcolemma and significantly improved the muscle resistance to lengthening contraction–induced muscle damage in the mdx mice compared with MD1. These results suggest that the incorporation of helix 1 of the coiled-coil motif in the CT domain of dystrophin to the microdystrophins will substantially improve their efficiency in restoring muscle function in patients with Duchenne muscular dystrophy.