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Congenital Disorders of the Neck
Published in Raymond W Clarke, Diseases of the Ear, Nose & Throat in Children, 2023
Previously known as ‘sternomastoid tumour’, this condition is characterised by torticollis and a lump in the sternomastoid muscle. The aetiology is unknown but it is most likely an idiopathic intense fibrosis of the muscle tissue. It presents in the newborn. Early recognition and intensive treatment with physiotherapy are essential to reduce the risk of permanent deformity of the neck.
Muscle Performance and Damage (Related to Exercise)
Published in Charles Theisler, Adjuvant Medical Care, 2023
Skeletal muscle comprises the largest organ system in the human body. Exercise-induced muscle injury most frequently occurs after unaccustomed exercise. The damage is characterized by ultrastructural alterations in muscle tissue, clinical signs, and symptoms (e.g., reduced muscle strength and range of motion, increased muscle soreness and swelling). Fortunately, muscle pain from overuse and most injuries is self-limited.
Resource-Limited Environment Plastic Surgery
Published in Mansoor Khan, David Nott, Fundamentals of Frontline Surgery, 2021
Johann A. Jeevaratnam, Charles Anton Fries, Dimitrios Kanakopoulos, Paul J. H. Drake, Lorraine Harry
Each tissue is variably susceptible to the mechanism of injury. Skin, the largest organ of the body, is particularly vulnerable to sheer and torsional forces, which disrupt the delicate network of vascular plexi that supply it from the underlying tissue planes. Large areas of skin can effectively be ‘degloved’ or lifted off the fascial and subfascial vasculature, struggling to survive. However, this may not be evident immediately and can take several days to evolve and declare itself as non-viable. The underlying fat is far more at risk from trauma compared to its durable cover. Fat is easily injured, often beyond the zone of skin injury. Necrosis quickly ensues once blood supply is interrupted, with the potential to form discrete nodules which undergo liquefactive necrosis. Muscle tissue can be bruised, sprained by stretch, or lacerated, with variable degrees of injury severity. It is extremely sensitive to direct trauma, where tearing and subsequent necrosis of the myofibrils creates space for haematoma formation and proliferation of inflammatory cells, as part of the repair process. Finally, nerve injury is well described and can be classified from mild bruising (neuropraxia) to complete disruption of the fascicles (neurotmesis), corresponding to cell death and loss of ability to transmit sensory or motor impulses.
Effect of muscle distribution on lung function in young adults
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2022
Wenbo Shu, Mengchi Chen, Zhengyi Xie, Liqian Huang, Binbin Huang, Peng Liu
A prolonged state of decline in VC results in hindered muscle function of the limbs, atrophy, weakness, and reduction of oxidative capacity (Bui et al. 2019; Shah et al. 2019). Swallow et al. found that the strength of the quadriceps muscle can predict the mortality of patients with moderate to severe COPD (Swallow et al. 2007). In addition to increasing the strength of the breathing muscles, exercise and training of the limbs can also enhance the contractility of the diaphragm, improve the elasticity of the thorax and alveoli, and improve lung compliance (Haas et al. 1985). All of the above are the correlation studies between lung function and limb function in patients with lung diseases. A strong positive correlation also exists between the strength of the flexor and extensor muscles of the lower limbs and the strength of the respiratory muscles in healthy people. The joint development of these parameters is conducive to improving the performance of athletes (Akınog˘Lu et al. 2019). Amann et al. (2010) found that the central brain commands, and the afferent feedback from the muscles of the limbs interact with each other, affecting the cardiopulmonary response. As such, limb function and respiratory function are closely related and affect the size of lung capacity. The role of limb muscle tissue is important.
Skeletal muscle plasticity and thermogenesis: Insights from sea otters
Published in Temperature, 2022
Traver Wright, Melinda Sheffield-Moore
Although the metabolic rate in resting skeletal muscle is low, it can rapidly increase to support metabolic demand. In skeletal muscle, this increased demand often powers muscle contractions for movement during physical activity, but can also increase for thermogenesis. Increased metabolic heat production can result from shivering (thermogenic muscle contractions that do not support functional movement), or nonshivering thermogenesis. Nonshivering thermogenesis has the advantage of not requiring muscle contraction to increase cellular energy expenditure. Instead, the sequestration of ions in membrane-bound intracellular chambers is made less efficient by “leaky” membranes. This leak requires additional energy expenditure to maintain trans-membrane concentration gradients, and includes proton leak across the inner mitochondrial membrane (where the proton gradient is used to generate ATP) as well as sarcolipin-mediated leak of sequestered calcium from the sarcoplasmic reticulum [4]. Through these mechanisms, skeletal muscle tissue contributes significantly to thermogenesis. Skeletal muscle metabolic capacity must be maintained at a level adequate to support not only thermogenesis, but also peak simultaneous demands for sustained physical activity and cellular maintenance. While increased demand for physical activity (e.g. endurance exercise training) is recognized as the primary work-producing stimulus to upregulate skeletal muscle aerobic capacity, the role of cold exposure is often underappreciated for its ability to stimulate an upregulation of metabolic capacity and thermogenic leak.
Identification of hub genes, miRNAs and regulatory factors relevant for Duchenne muscular dystrophy by bioinformatics analysis
Published in International Journal of Neuroscience, 2022
Meng-Xi Xiu, Bin Zeng, Bo-Hai Kuang
Duchenne muscular dystrophy (DMD), one of the most severe muscle disorders, is a genetic disorder caused by a mutation in the gene encoding dystrophin protein on the X chromosome (Xp21.2) [1,2]. Dystrophin protein is the main component of the dystrophin glycoprotein complex (DGC), linking the muscle cell cytoskeleton to the extracellular matrix [3]. The absence of dystrophin protein leads to the eventual collapse of muscle cell membranes, causing severe muscle damage, and normal muscle tissue is gradually replaced by fibrofatty tissue. DMD patients exhibit typical symptoms at the age of 3–5 and most require a wheelchair at the age of 11–12 [4]. In the third decade of life, most DMD patients die due to cardiorespiratory failure [5]. Due to the lack of specific biomarkers for the prediction of disease progression and therapeutic targets for accurate treatment, windows of opportunity for drug or surgical interventions in DMD patients are generally missed, consequently resulting in increased risk of death [6].