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Everett Bailey
Everett Bailey

Hot Mature Muscle

Caveolin-3, the muscle-specific isoform of the caveolae-associated protein caveolin, is often thought to be localized exclusively in the surface membrane in mature fibers and associated with transverse (t)-tubular system only transiently during development. Skeletal muscle fibers present a model where the surface membrane (sarcolemma) can be completely separated from the cell by mechanical dissection. Western blotting of matching portions of individual fibers from adult rat muscle in which the sarcolemma was either removed (skinned segment), or left in place (intact segment), revealed that > or = 70% of caveolin-3 is actually located deeper in the fiber rather than in the sarcolemma itself. Triton solubility of caveolin-3 was no different between sarcolemmal and t-tubule compartments. Confocal immunofluorescence microscopy showed caveolin-3 present throughout the t-system in adult fibers, with 'hot-spots' at the necks of the tubules in the sub-sarcolemmal space. A similar representation was seen for the muscle specific voltage-dependent sodium channel Nav1.4 and it was found that at least some Nav1.4 co-immunoprecipitated with caveolin-3 in skinned muscle fibers. The caveolin-3 hot-spots just inside the opening of t-tubules may form regions that localize ion channels and kinases at the key place needed for efficient electrical transmission into the t-tubules as well as for other signaling processes.

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Muscle has limited capacity for regeneration following injury, and part of the healing is achieved by scar tissue formation, which is in turn frequently related with the volume of muscle necrosis and the size of the haematoma. The presence of an intramuscular scar alters the normal muscle contraction vector reducing strength and increasing fatigue. Hence, the more severe is an injury, the more muscle biomechanics will be altered and muscle fatigue will be increased, resulting in an augmented risk of re-injury [1].

Relapses represent the most frequent complications of muscle injuries; they are generally favoured by diagnostic errors and improper treatment, particularly concerning the timing of return to activity. Recurrences represent a major topic in sport medicine: a prompt return to physical activity and a favourable recovery are the main challenge that the physician and the athlete have to deal with, particularly in the elite athlete [2, 3].

Factors associated with recurrent muscle injuries include: extrinsic and intrinsic factors. Extrinsic factors are premature return-to-play, inadequate training, muscle strength imbalances, decreased flexibility, increasing age, and history of prior injury. Intrinsic factors are persistent weakness in the injured muscle, reduced extensibility of the musculo-tendon unit due to residual scar tissue and adaptive changes in the biomechanics and motor patterns of sporting movements following the original injury [11, 13].

Myositis ossificans formation is a two-step process. The first step consists of degeneration and necrosis of the muscular tissue and occurs 1 or 2 weeks after the injury (early MO), while the second step is mesenchymal cell proliferation and bone formation and occurs 3 or 4 weeks after the injury (mature MO).

US has been proposed as a reliable method to diagnose MO. At US, MO appears as homogenous, hypoechoic, well-defined oval-shaped mass, with regular borders, with thickening of the surrounding muscle belly. A hyperechoic, ill-defined lamellar rim could be observed in early MO, while in mature stage a more defined rim with acoustic shadowing could be seen [1] (Fig. 3).

Ultrasonography findings of MO nevertheless are non-specific and can easily be confused with a soft-tissue sarcoma. In doubtful cases, a short-term follow-up is recommended to highlight the typical US changes that occur from early to mature MO [17].

Pyomyositis usually affects the large muscles of the lower extremities or trunk. The illness typically unfolds over several weeks. Most patients present with pain and tenderness localized to the body of a muscle, but occasionally patients will present with acute illness with marked systemic toxicity [19, 20].

Transverse sonogram of a patient with pyomyositis of the rectus femoris muscle. Diffuse muscle swelling and partial posterior acoustic enhancement can be seen, suggesting a gas-forming organism infection

US of affected muscles shows muscle swelling with thickened myofibrils with loss of muscle striation (Fig. 5). Muscle may appear inhomogenously hypoechoic with hypoechoic pockets surrounding muscle, representing inflammatory fluid [4, 15].

Concerning fibrotic scar formation, the gap between the damaged muscle fibres is readily filled with a haematoma. In the first days after trauma an inflammatory response is created with phagocytes recalling and invading the lesion. The first clot is then organized and it will act as an initial web at which fibroblasts will be anchored. This newly formed tissue allows blocking lesion expansion. Fibroblasts start to produce type I collagen, thus creating a solid structure that will become the strongest point of the traumatized muscle tissue in about 10 days. Over time, the scar will tend to decrease the volume [1, 15].

On US, normal muscle tissue may be seen protruding through a focal epimysial defect (Fig. 7). A dynamic study with contraction of the muscle under evaluation permits to identify a defect in perymisium through which muscle bulges with contraction.

a Patient with a lower leg muscle hernia. A lump can be observed in the lateral part of the lower leg. b Sagittal sonogram of the same patient. Muscle tissue can be seen protruding through an epymisial defect

Vision occurs when light is processed by your eye and interpreted by your brain. Light passes through the transparent eye surface (cornea). It continues through the pupil, the opening to the inside of the eye. The pupil becomes larger or smaller to control the amount of light that enters the eye. The colored part of the eye is called the iris. It is a muscle that controls pupil size. After light passes through your pupil, it reaches the lens. The lens focuses light on your retina (the back of the eye). The retina converts light energy into a nerve signal that the optic nerve carries to the brain, where it is interpreted.

All of the eye structures change with aging. The cornea becomes less sensitive, so you might not notice eye injuries. By the time you turn 60, your pupils may decrease to about one third of the size they were when you were 20. The pupils may react more slowly in response to darkness or bright light. The lens becomes yellowed, less flexible, and slightly cloudy leading to the development of cataracts. The fat pads supporting the eyes decrease and the eyes sink into their sockets. The eye muscles become less able to fully rotate the eye.

The sense of touch makes you aware of pain, temperature, pressure, vibration, and body position. Skin, muscles, tendons, joints, and internal organs have nerve endings (receptors) that detect these sensations. Some receptors give the brain information about the position and condition of internal organs. Though you may not be aware of this information, it helps to identify changes (for example, the pain of appendicitis).

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For many years, the extracellular matrix was thought to be created by connective tissue cells and surround those cells as a mere structural scaffold. The extracellular matrix was categorized as a stable inert support material that was independent from cellular activity. We now know that after the cell produces and secretes the extracellular matrix macromolecules, the cell continues to interact with the extracellular matrix and as development proceeds the molecular composition of the extracellular matrix changes in a precisely regulated fashion. Therefore, the fate of the cell in terms of its cytoskeletal organization, migration, proliferation and differentiation are related to the compositional properties of the extracellular matrix. These changes in the extracellular matrix alter the physical properties of the tissue or organ in terms of flexibility and mechanical strength. During the past decade, knowledge of the number and complexity of extracellular matrix macromolecules has significantly expanded. However, their role in tissue growth, structure, and function is somewhat an enigma. Research addressing the influence of the extracellular matrix on muscle development is in its infancy. It is now known that the extracellular matrix plays a role in skeletal muscle development, the regeneration of muscle, and in the development of cardiovascular disease. In this issue of Basic and Applied Myology, these emerging areas of research are highlighted. The papers by Carrino, Poussart et al., and Brandan and Larrain discuss skeletal muscle and connective tissue development. The genetic regulation of skeletal muscle development and its surrounding connective tissue is not well understood. These papers explore the dynamic expression of proteoglycans, the role of heparan sulfate proteoglycans in terminal skeletal muscle differentiation, and the potential influence of a key growth factor on connective tissue formation. In addition to the extracellular matrix playing a critical role in the formation of skeletal muscle, Grounds et al. describe changes in the expression extracellular matrix components with the progression of skeletal muscle regeneration in vivo. During the repair and regeneration of skeletal muscle, myogenic satellite cells are activated. Velleman et al. report the presence of a satellite cell produced heparan sulfate proteoglycan. Despite a decrease in mortality from heart disease since the 1960's, cardiovascular disease remains a primary cause of death. Many complex factors lead to the onset of cardiovascular disease. It is now known that the extracellular matrix undergoes significant changes during the progression of various cardiac pathologies which may contribute to increased stiffness and enlargement of the heart. Papers by McCormick and Thomas, and Medeiros and Shiry discuss extracellular matrix changes that occur in the myocardium. The muscle foods industry comprises a significant part of the agricultural economy. Tenderness is an important factor by which consumers judge muscle food quality and is influenced by connective tissue. In the paper by Eggen et al. a possible role of chondroitin/dermatan sulfate proteoglycans in post mortem meat tenderness is discussed. It is impossible in an issue of this nature to report on all aspects of muscle extracellular matrix biology. Emerging areas of significant biological impact have been addressed by leaders in their respective fields. We hope, this issue provides a strong survey of these areas and stimulates further scientific investigation. 041b061a72

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