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Molecular Mechanisms of Training Effects
Published in Atko Viru, Adaptation in Sports Training, 2017
The above-presented data are collectively rather conclusive that (a) training exercises stimulate an enlargement of cellular structures and correspondingly increase the contents of various proteins, and (b) these processes are specifically related to the training exercises used. Differences in training effects suggest that in the training process the adaptive protein synthesis is utilized in many ways. The main locus of the adaptive protein synthesis varies between tissues and organs. In striated muscle tissue different distribution of the adaptive protein synthesis exists between muscles, and within a muscle between motor units (types of muscle fiber). Within a cell, the adaptive protein synthesis is differently distributed between cellular structures and between individual proteins. In all cases there exist two main determinants of the distribution of the adaptive protein synthesis: The rate of functional activities during exercise performance or in the first stage of the recovery periodThe significance of the organ, muscle, motor unit, cellular structure, and metabolic pathway in acute adaptation to the performed exercise and in the realization of the concrete motor task
Discussions (D)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Most authors of recent textbooks in clinical neuroscience do not mention the term “myotomes,” nor do many authors of recent textbooks in basic neuroanatomy. Most authors who do mention the term use it to label only embryological structures (e.g., W&W, p. 118, 154–155, 1084,[120–112],- K&S, p. 545, Brod, p. 449; n&d, p. 126 [Fig, 4–21]; CH&L, p. 61). The remainder, however, also use the term “myotomes” to label mature striated muscle tissue/fibers derived from the embryological myotomes.
The movement systems: skeletal and muscular
Published in Nick Draper, Helen Marshall, Exercise Physiology, 2014
Cardiac and skeletal muscle are striated (striped) in appearance, meaning they have microscopic light and dark patches within their structure. These striations are due to the specific arrangement of the proteins that enable muscular contraction. This will become clearer when the structure of skeletal muscle is discussed in the following section. As can be seen from Figure 5.8, smooth muscle is the only non-striated muscle tissue. While skeletal muscle tissue is multi-nucleate, due to its relatively long fibres, cardiac and smooth muscle fibres are shorter and have only one nucleus.
Treatment options from bench to bedside for adult dermatomyositis
Published in Expert Opinion on Orphan Drugs, 2020
Samuel Katsuyuki Shinjo, Fernando Henrique Carlos de Souza
Although skeletal striated muscle tissue is the main target in DM, its involvement is often accompanied by tissue and/or organ impairment as a result of systemic inflammatory processes [4,5]. Therefore, muscle involvement, as well as cardiac, pulmonary, gastrointestinal, articular, and cutaneous impairments, is possible [1,2,4,5]. Because of these systemic manifestations associated to a variety of DM manifestations, there is a patient management challenge in clinical practice. Further myositis-specific autoantibodies may be associated with characteristic clinical features along the DM spectrum [6]. Therefore, these autoantibodies can help to better characterize DM phenotypes and consequently guide clinical care and establish that some DM patients are, e.g., at greater risk to cutaneous (e.g., anti-Mi-2 and anti-MDA-5), lung (e.g., anti-MDA-5) or systemic diseases and to neoplasia (e.g., anti-NXP-1 and anti-TIF-1↖?); therefore, it is important to establish appropriate therapy and follow-up.
Safety and feasibility of arterial wall targeting with robot-assisted high intensity focused ultrasound: a preclinical study
Published in International Journal of Hyperthermia, 2020
M. H. A Groen, F. J. B Slieker, A. Vink, G. J. de Borst, M. V. Simons, E. S. Ebbini, P. A. Doevendans, C. E. V. B. Hazenberg, R. van Es
For the animals with a follow up period, not all slices showed histological effects, as one would expect considering the cutting process. However, for all FUP animals at least one slide per animal showed histological changes. In the cases where the effect of the treatment was histologically visible, different stages of tissue damage and scar tissue formation were observed after 3 and after 14 days FUP. After 3 days FUP, fibrinoid changes with presence of macrophages were observed in the soft tissue between the femoral artery and vein and the adventitial layer of the femoral artery (Figure 5). In addition, focal necrosis of the adjacent striated muscle tissue with inflammatory reaction was observed. In one artery, pyknosis of some smooth muscle cells in the outer layer of the media was observed. After 14 days FUP, discrete scar tissue lesions with abundant fibroblasts were observed in the soft tissue around the artery, the adventitial layer and in a few cases the outer part of the media. In some animals, small scars were observed in the adjacent striated muscle tissue (Figure 6). In one animal there was limited histological damage to a nerve next to the artery with giant cell reaction.
Novel Mutation of the Dystrophin Gene in a Child with Duchenne Muscular Dystrophy
Published in Fetal and Pediatric Pathology, 2018
Jingjing Jiang, Tiejia Jiang, Jialu Xu, Jue Shen, Feng Gao
Duchenne muscular dystrophy (DMD MIM#310200) is an allelic X-linked recessive disorder caused by mutations in DMD gene which encodes dystrophin. DMD affects approximately 1/3500 live male newborns (1). Female carriers of the DMD gene are usually asymptomatic or show mild symptoms. Gene mutations affect the expression of dystrophin in striated muscle tissue, resulting in progressive degeneration and necrosis of the proximal limb muscles. The majority of children have a bilateral pseudohypertrophy of the gastrocnemius muscle. This is due to the atrophy of the muscle fibers, which then are filled with fat, the strength of the muscle is weakened, but it is hard to the touch. The typical clinical manifestation is retrogression of motor development. Patients have a special “duckstep” gait, proximal muscle weakness, calf hypertrophy, weak tendon reflexes, positive Gower sign, increased serum creatine kinase (CK), while the myocardial cells undergo progressive damage. The onset age of DMD in children is generally between 3 and 5 years of age, is progressive, with loss of independent ambulation before age 13. Death is often from respiratory failure and/or heart complications at about 20 years of age.