650 research outputs found

    Molecular gyroscopes and biological effects of weak ELF magnetic fields

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    Extremely-low-frequency magnetic fields are known to affect biological systems. In many cases, biological effects display `windows' in biologically effective parameters of the magnetic fields: most dramatic is the fact that relatively intense magnetic fields sometimes do not cause appreciable effect, while smaller fields of the order of 10--100 μ\muT do. Linear resonant physical processes do not explain frequency windows in this case. Amplitude window phenomena suggest a nonlinear physical mechanism. Such a nonlinear mechanism has been proposed recently to explain those `windows'. It considers quantum-interference effects on protein-bound substrate ions. Magnetic fields cause an interference of ion quantum states and change the probability of ion-protein dissociation. This ion-interference mechanism predicts specific magnetic-field frequency and amplitude windows within which biological effects occur. It agrees with a lot of experiments. However, according to the mechanism, the lifetime Γ−1\Gamma^{-1} of ion quantum states within a protein cavity should be of unrealistic value, more than 0.01 s for frequency band 10--100 Hz. In this paper, a biophysical mechanism has been proposed that (i) retains the attractive features of the ion interference mechanism and (ii) uses the principles of gyroscopic motion and removes the necessity to postulate large lifetimes. The mechanism considers dynamics of the density matrix of the molecular groups, which are attached to the walls of protein cavities by two covalent bonds, i.e., molecular gyroscopes. Numerical computations have shown almost free rotations of the molecular gyros. The relaxation time due to van der Waals forces was about 0.01 s for the cavity size of 28 angstr\"{o}ms.Comment: 10 pages, 7 figure

    Use of branched-chain amino acids for reducing exercise-caused skeletal muscle damage

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    Introduction: Skeletal muscles damage (direct and vicarious) slows down the recovery processes in patients with injuries of the musculoskeletal system. It occurs in the early postoperative period as well. An increase in the rigidity of the skeletal muscle extracellular matrix can reduce pain, tissue swelling, and accelerate the recovery of contractility.Objective: The analyses of the effect of branched-chain amino acids (BCAAs) intake on the expression of IGF1 genes, type 1, 3 and 5 collagen, which are crucial in the composition of the skeletal muscle extracellular matrix, as well as on the muscle membrane damage against the background of chronic damage to skeletal muscles.Material and methods: 12 young healthy male subjects, skiers aged 19 (18; 22) received a placebo treatment (maltodextrin, 100 mg/kg body weight/day; n = 6) or a mixture of amino acids (leucine, isoleucine, valine – 50:25:20 mg/kg body weight/day respectively; n = 6). The treatment was received daily against the background of a large amount of aerobic high-intensity training (up to 22 hours per week). Before and after the amino acids intake a biopsy of the musculus vastus lateralis was performed, and venous blood samples were taken during the experiment.Results: The intake of leucine against the background of training led not only to a pronounced increase in the level of IGF1 protein in blood by 1.5 times (which corresponds to the literature data), but also to a trend towards an increase in the expression of IGF1Ea mRNA by 1.8 times in the skeletal muscle, and a decrease in the level of markers of muscle membranes damage – creatine phosphokinase (CPK) activity and myoglobin. In addition, changes in the IGF1-dependent collagen genes expression strongly correlated with changes in IGF1Ea expression, but not with IGF1 protein in blood (pooled group, n = 12). Thus, the intake of leucine as a part of the essential amino acids can reduce damage to skeletal muscles caused by excessive physical activity, lack of physical activity, or direct trauma.Conclusion: A 10-week BCAAs intake by individuals with documented chronic muscle membrane damage caused an increase of basal levels of IGF1 in blood and a trend towards increased IGF1Ea mRNA expression in skeletal muscle, and also caused a modest reduction in damage of skeletal muscle membrane
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