China 
Africa 
Explore chapters and articles related to this topic
Muscle Physiology and Electromyography
Published in Verna Wright, Eric L. Radin, Mechanics of Human Joints, 2020
The action potential sweeping over the surface of the muscle causes a response in the contractile system by the process of excitation-contraction coupling. Between the myofibrils are sacs of sarcoplasmic reticulum, and the surface of thesarcolemma frequently invaginates, giving rise to ‘T tubules,” so called because they traverse the muscle fibers (see Fig. 9). A T tubule and its surrounding sarcoplasmic reticulum are collectively termed a triad, but although they are closely associated with the sarcoplasmic reticulum, the T tubules are not connected to it. In human muscle, the triads are located at the boundary of the A and I bands of the sarcomeres (10). As the action potential sweeps over the surface of the muscle, the depolarization spreads down the T tubules. In response to the action potential, the sarcoplasmic reticulum releases calcium ions into the myoplasm. The free calcium initiates the mechanical events of a contraction, and the contraction is subsequently turned off when the calcium is removed from the binding sites. Although in the process of a contraction some calcium ions may become bound to other myoplasmic proteins, they are all eventually returned to the internal compartment of the sarcoplasmic reticulum by a calcium ATPase resident in the membrane of the sarcoplasmic reticulum, to arm the system for the next contraction (11).
Calcium Electroporation – A Novel Treatment to Overcome Cancer-Mediated Immune Suppression
Published in Marko S. Markov, James T. Ryaby, Erik I. Waldorff, Pulsed Electromagnetic Fields for Clinical Applications, 2020
The plasma membrane calcium-ATPase (PMCA1–4) pumps are a family of ATP-driven pumps which play an important role in calcium homeostasis. PMCA1 is ubiquitously expressed, while PMCA2–4 are expressed in a cell- and tissue-dependent manner (Padányi et al., 2016). Modified expression of these channels has been observed in malignant cells, although not in a straightforward manner. Upregulation of PMCA1 and PMCA2 and downregulation of PMCA4 has been reported in breast cancer cell lines (Curry, Roberts-Thomson, & Monteith, 2011; Monteith, Davis, & Roberts-Thomson, 2012; Padányi et al., 2016). PMCA4 is also downregulated in colon carcinoma (Cui et al., 2017; Curry et al., 2011; Padányi et al., 2016), while PMCA1 has been found to be upregulated in oral squamous cell carcinoma (Cui et al., 2017).
Computational modeling of inhibitory signal transduction in urinary bladder PDGFRα+ cells
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2023
Amritanshu Gupta, Rohit Manchanda
We see from Figure 2a that the fraction of activated G-protein increases with an increase in the intensity of the ATP stimulus. This results in an enhancement in the production of IP3 in the cytosol (Figure 2b). Elevated IP3 releases Ca2+ from the ER via the IP3R receptors, followed by the uptake of Ca2+ from the cytosol back into the ER by the sarcoendoplasmic reticulum calcium ATPase (SERCA) pump. Due to the difference in the temporal response of the IP3R and the SERCA pump, Ca2+ transients of varying amplitude are set up in the cytosol, as seen in Figure 2c. The Ca2+ transients, in turn, activate the SK3 channels, resulting in outward hyperpolarizing potassium currents (ISK3). As seen in Figure 2d, the outward-flowing K+ currents match in amplitude with the peak values of the SK3 currents simulated by Yeoh et al. (2016), represented by black circles.
Association between polymorphism and haplotype of ATP2B1 gene and skeletal fluorosis in Han population
Published in International Journal of Environmental Health Research, 2023
Yue Gao, Yang Liu, Yuting Jiang, Ming Qin, Zhizhong Guan, Yanhui Gao, Yanmei Yang
High fluoride exposure leads to abnormal calcium metabolism, fluoride can cause the opening of cell membrane Ca2+ channels and an increase in intracellular Ca2+. Moreover, calcium regulates numerous extracellular and intracellular processes (Ciosek et al. 2021), and it is required for bone formation, growth, and maintenance, as well as the cellular cytoskeleton’s integrity. Intracellular Ca2+ signaling has been found to govern numerous activities in osteoblasts, osteoclasts, chondrocytes, and nerve terminals (Lieben and Carmeliet 2012). Abnormalities in genes involved in Ca2+ signaling will affect bone structure or lead to diseases of bone function (Blair et al. 2007). ATP2B1, which encodes plasma membrane calcium ATPase (PMCA) 1, is one of the candidate genes for hypertension. PMCAs are ATP-driven, calcium-ion-extruding pumps that control intracellular calcium levels by extruding calcium ions from cells (Little et al. 2016). It maintains intracellular Ca2+ concentration by regulating intracellular/extracellular Ca2+ homeostasis (Hirawa et al. 2013). As a result, ATP2B1 may be involved in regulation of calcium ions during the development of fluorosis, affecting the susceptibility of skeletal fluorosis, so to carry out this research.
Redox homeostasis in sport: do athletes really need antioxidant support?
Published in Research in Sports Medicine, 2019
Ambra Antonioni, Cristina Fantini, Ivan Dimauro, Daniela Caporossi
N-acetylcysteine (NAC) is a reduced thiol donor and redox modulator. Its chemical structure derives from the amino acid L-cystein and it is able to enhance availability of cysteine and glutathione (GSH) in muscle (Medved et al., 2004). For this reason, NAC is considered an effective non-specific antioxidant that potentially reduces the harmful effects of exercise-induced ROS (Medved et al., 2004). Beside its pharmacological application as mucolytic agent, NAC is utilized among nutritional additives for athletes as a means of improving recovery and enhancing athletic performance. Proposed mechanisms of NAC action include enhancement of potassium homeostasis, preservation of the NA+/K+ pump activity within skeletal muscle and the inhibition of calcium ATPase oxidation at the sarcoplasmic reticulum (Ferreira & Reid, 2008). However, both Gomez-Cabrera (2015) and Trewin (2015) groups described at molecular level that NAC supplementation can affect canonical skeletal signaling pathway (i.e. JNK, p65phox, Akt/mTOR) reducing both the expression of proteins implicated in exercise-induced adaptation and limiting the activity of specific kinases such as p38MAPK, Akt or p70s6K.