The success was remarkable, according to the researchers: Even muscles that had already lost half of its mass, recovered visible. (Leppanen et al. p5549-65) At the same time, the mice survived for several weeks longer than their untreated counterparts and also developed a healthy appetite again. (Mantovani, p296) The new study is therefore interesting in two respects: First, it demonstrates that the muscle loss at least in animal models in fact, affects the chances of survival, and secondly, it shows a way, may be how to prevent this degradation, and even reversed. (Bruera et al. p857)

Muscle atrophy

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Muscle atrophy is a medical term that refers to the decrease in the size of skeletal muscle, losing muscle strength because of the strength of muscle is related to its mass. (Burnfoot, p323-34)

All changes in cell morphological character may affect isolated cells or groups of them, therefore the modification of a whole tissue. (Bhattacharyya et al. p56-78) All stimuli that may act on a cell are actually functional stimuli: when they exceed the physiological limits may injure the cell to reverse the processes of life, or cause significant modifications regressive. (Warmolts, p374-79)

The atrophy is therefore the morphological expression of a functional and structural involution of a cell or tissue. It is an acquired deficiency, which normally involves a preexisting cellular and tissue, and for that reason must be distinguished from hypoplasia of the aplasia and agenesis. (Warmolts, p374-79) Moreover, the atrophy must be distinguished from a disease that entails structural reduction of an organ, or part thereof due to a necrotic destructive process, in which case there is a massive cell death. (Ryan et al. p355-63)

There are several diseases and disorders that cause a decrease in muscle mass, including inactivity, cachexia present in patients with cancer or heart failure, chronic obstructive pulmonary disease, extensive burns, liver failure, electrolyte disturbances, anemia. Others can cause muscle wasting syndromes such as malnutrition, denervation of motor neurons and in spinal muscular atrophy of childhood and the inflammatory myopathies and dystrophies, among others. (Warmolts, p374-79)

In the microscopic appearance are three main types of atrophy, simple atrophy, degenerative atrophy and atrophy number. Simple atrophy is a decrease in the volume of muscle components leads to shrinkage or reduction in size of the tissue and organ. (Bhattacharyya et al. p56-78) Atrophy is more common, affecting more differentiated cells. It can be seen during the prolonged fast in almost all body tissues, mainly in muscle tissue. (Fearon et al. p1345-50)

Numerical atrophy exists when the disappearance of cellular elements causes the decrease in the volume of an organ, the volume reduction is progressive and proportional to the number of cells and tissues normally affects labile elements.

In degenerative atrophy can see big changes to the cytoplasm and nucleus of cells and organ tissue. This process can lead to the occurrence of necrosis. (Bhattacharyya et al. p56-78) In all cases of atrophy, the cytoplasm is the most affected is almost always a reduction in quantity of it, so much so that, observing the atrophic tissue under a microscope can distinguish a discrete cell densification caused by the reduction uniform cell volume. (Leppanen et al. p5549-65) These changes are accompanied by profound alterations in cytoplasmic, turbidity, presence of pigment granules and decreased number of mitochondria. (Ryan et al. p355-63)

There are several diseases and disorders that cause a decrease in muscle mass, including inactivity, as in the sedentary (do nothing) or a cast- cachexia or body wasting syndrome present in patients with cancer or heart failure, chronic obstructive pulmonary disease, extensive burns, hepatic disorders, electrolyte, anemia, etc. Other syndromes can cause muscle atrophy such as malnutrition, denervation of neurons in the motor and spinal muscular atrophy of childhood and myopathies and inflammatory dystrophies, among others. (Conlisk et al. p1051)

Mechanisms of action

To understand what happens in a muscle of a patient with muscular dystrophy is useful to recall, albeit brief summary, it is done and how a normal muscle. (Leppanen et al. p5549-65) It consists of a central part of the contractile (muscle belly) and from one end device (tendon) that ensures contact with the bony surface of the muscle. The tendon ends can be of various shape: when the muscle is inserted by two tendons to bone is called the biceps, triceps tendon with three, four quadriceps. (Dunlop, p76-82)

The muscle is the engine that ensures each form of motion of our body and this happens through the contractile activity that allows the movement of bone segments with which the muscle makes contact. (DeWys, p491-97)

When a muscle contraction produces a motor effect for an individual defines this muscle is agonist. When the contracts ‘agonist, is released at the same time that the muscle action contrary (the’ antagonist) (Bhattacharyya et al. p56-78) for example, when you want to flex the forearm is active as an agonist, the biceps and, simultaneously releasing the triceps brachii and if you want to do the opposite movement, ie to extend the forearm, then the pattern is reversed: the biceps relaxes and the triceps contracts. (Eigler, p487)

If this is not balanced equilibrium and the agonist and antagonist muscles contract simultaneously has the so-called phenomenon of “co-contraction,” which occurs in certain pathological conditions where there is spasticity (but which can be determined even under normal conditions, such as Alert sharp reactions in the face of a sudden perception of danger). (Gagnon, p675-88)

Galectins and galectin

Galectin 1 is a protein overexpressed by many cancers; it is involved in multiple processes of tumor development including tumorigenesis, proliferation and migration of tumor cells and their metastasis, resistance to radiation and chemotherapy, their escape the immune system or angiogenesis. (Leppanen et al. p5549-65)

The nature of the receptor-against galectin-1 that is involved in the establishment of the synapse between the pre-B cells and stromal cells remains to be determined. (Feingold, p184-90) However, the cons-receptor galectin-1 has been identified in other biological systems: these extracellular matrix proteins (laminin and fibronectin) or surface receptors such as CD45, CD43, CD7, CD2, CD3 or GM1. GAL1 is involved in many biological functions such as adhesion, growth and cell death. (Song et al. p36-47)

GAL1 and cons-receptors act as potent regulators of homeostasis of the immune system, and these are the signals delivered by the various cons-receptors that determine the nature of biological responses. (Leppanen et al. p5549-65) The galectins induce contrasting effects on cell growth and the biological effect observed proliferation or apoptosis depends on the cell type and cell activation status. (Hengge, p129-38) For example, it was reported that GAL1 could both play a role in inhibition of proliferation of T cells and promote proliferation of vascular endothelial cells. Galectins also play a crucial role in the process of cell transformation and metastasis formation. (Dias-Baruffi et al., p114-49)

Under the microscope, the muscle is composed of a set of muscle fibers that are surrounded by a connective membrane is called the sarcolemma. (Hengge, p129-38) Each muscle fiber, in turn, is composed of a thousand myofibrils, which represent the fundamental contractile unit. (Leppanen et al. p5549-65) These myofibrils have an average length of 40-50 microns and a diameter of just one micron. (Feingold, p184-90)

To be able to contract, the muscle needs a command: This command comes through nerve endings that make contact with the muscle belly through the endplate, which is the terminal part of the neuron that is linked to the muscle fiber. (Grinspoon, p634-36)

In the case of a voluntary movement (for example, take a bucket and lift it off the ground), the order from the cerebral cortex, travels along nerve fibers to the core, and then continues towards the periphery from the bone until it reaches the muscles against are able to ensure the desired motor action (in our example, grasp the handle of the bucket and lift it). (Hengge, p129-38)

The muscles, however, are able to provide even involuntary movements, ie those that are carried out automatically or reflected (and, anyway, beyond our specific desire). And ‘the case of the muscles that provide respiration, urination, etc. (Maguid, p843-57)

What happens in the case of muscular dystrophy? In this disease, the muscle undergoes a slow process of degeneration, characterized by necrosis (from the greek = dead) of muscle fibers and the concomitant appearance of fibrosis, or by replacement of normal contractile tissue of the muscle connective tissue. (Maguid, p843-57) The latter consists of fibers that have no ability to contract, for which the muscle slowly loses its function and the patient begins to experience progressive weakness. (Rowe, p623-24)

Note that the muscles of patients with muscular dystrophy does not appear to decrease in volume but on the contrary, some muscles – such as those of calves – you can have even more voluminous than normal (pseudohypertrophy) precisely because of fibrosis and the accumulation of adipocytes (fat cells) going to replace degenerated muscle cells. (Holroyde, p78) In addition to the muscles in DMD are…

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