The static preload associated myogenic spontaneous fasciculation response in lengthening cardiac muscle

The passive tension force enhancement is one kind of myogenic spontaneous fasciculation in muscles. However, its physiological properties in cardiac fibres are not well known. In this study, mice cardiac papillary muscle spontaneous force enhancement was evaluated by micro stepping stretch method. The occurrence of spontaneous force and real time cardiac fibre Ca2+ redistribution was tranced by Flou-3 (2mM) indicator. Force enhancement amplitude, enhancement prolonging time, and tension–time integral were analysis by myograph analyser. The results indicated that the spontaneous force occurred immediately after the active stretch, rapidly enhanced during tolerating the sustained static stretch. The force occurrence and amplitude enhance synchronized with the Ca2+ recruitment and lightning transmitted to adjacent fibres. In high preload fibres, the enhancement was forceful to over its maximum passive tension (6.20 ± 0.51 N/mm2 to 4.49 ± 0.43 N/mm2). The force occurrences were unsteadiness in each stretch. The increased enhancement amplitude combining with the shortening prolonging time induced reduction of tension–time integral. We concluded that the intracellular Ca2+ synchronized force enhancement is one kind of interruption event in overloading cardiac fibres. This interruption occurred during the relaxation processing in cardiac muscle, therefore affect the rhythmic stability of cardiac relaxation-contraction cycle.

Effectiveness of Plyometric and Eccentric Exercise for Jumping and Stability in Female Soccer Players—A Single-Blind, Randomized Controlled Pilot Study

Hamstring muscle injury is common in female soccer players. Changes affecting eccentric strength, flexibility, and the quadriceps–hamstring contraction cycle are risk factors associated with this type of injury. Methods: Seventeen soccer players were randomized to two groups: experimental (plyometric and eccentric exercises without external loads) and control (eccentric exercises without external loads). Eighteen sessions were scheduled over 6 weeks. The exercise program included three plyometric exercises (single-leg squat and lunge, 180 jump, and broad jump stick landing) and three eccentric exercises (Nordic hamstring exercise, diver, and glider). Dependent variables were jumping height (My Jump 2.0 App) and anterior, posteromedial, and posterolateral lower limb stability (Y-Balance test). Results: Following intervention, improvements were found in anterior and posteromedial stability (p = 0.04) in the experimental group. Posterolateral stability improved in athletes included in the control group (p = 0.02). There were differences in the repeated measures analysis for all variables, with no changes in group interaction (p > 0.05). Conclusions: Eccentric exercises, either combined with plyometric exercises or alone, can improve lower limb stability. No changes in jump height were noted in either group. There were no differences between the two groups in the variables studied. Future studies should analyze the effect of external loads on jumping stability and height in the performance of plyometric exercises.

Cryo-electron tomography of cardiac myofibrils reveals a 3D lattice spring within the Z-discs

The Z-disc forms a boundary between sarcomeres, which constitute structural and functional units of striated muscle tissue. Actin filaments from adjacent sarcomeres are cross-bridged by α-actinin in the Z-disc, allowing transmission of tension across the myofibril. Despite decades of studies, the 3D structure of Z-disc has remained elusive due to the limited resolution of conventional electron microscopy. Here, we observed porcine cardiac myofibrils using cryo-electron tomography and reconstructed the 3D structures of the actin-actinin cross-bridging complexes within the Z-discs in relaxed and activated states. We found that the α-actinin dimers showed contraction-dependent swinging and sliding motions in response to a global twist in the F-actin lattice. Our observation suggests that the actin-actinin complex constitutes a molecular lattice spring, which maintains the integrity of the Z-disc during the muscle contraction cycle.

Alat Pendeteksi Detak Jantung dan Kesehatan Berbasis Arduino

The heart is a human organ that pumps blood. The heart contracts, where one contraction cycle is usually called a heartbeat. Calculation of heart rate is often done manually by counting the pulse on the wrist for one minute. This method is considered inaccurate because it only relies on the human sense of touch. By making it easier to calculate the heart rate with the Electrocardiograph (ECG) device only but this tool is used in hospitals and cannot be moved. With a sensor that makes daily activities easier. For example, a pulse sensor that is easily available is a pulse sensor that can be used to detect the human heartbeat. With the heart rate device that can be moved using a pulse sensor. Where in the tool that in this final project detects the heart rate will be displayed on the Liquid Crisytal Display (LCD) where the detection results displayed are the results of the detection of human heartbeats accompanied by diseases that may be experienced from heart rate abnormalities.

Cryo-electron tomography of cardiac myofibrils reveals a contraction-induced lattice twist in the Z-discs

The Z-disc forms a boundary between sarcomeres, which constitute structural and functional units of striated muscle tissue. Actin filaments from adjacent sarcomeres are cross-bridged by α-actinin in the Z-disc, allowing transmission of tension across the myofibril. Despite decades of studies, the 3D structure of Z-disc has been elusive due to the limited resolution of conventional electron microscopy. Here, we observed porcine cardiac myofibrils using cryo-electron tomography and reconstructed the 3D structures of the actinactinin cross-bridging complexes within the Z-discs in relaxed and activated states. We found that the α-actinin showed a contraction-induced swing motion along with a global twist in the actin lattice. Our observation suggests that the elasticity and the integrity of the Z-disc during the muscle contraction cycle are maintained by the structural flexibility within the actin-actinin complex.

Synthesis and Light-Induced Actuation of Photo-Labile 2-Pyridyl-1,2,3-Triazole Ru(bis-bipyridyl) Appended Ferrocene Rotors

To realise useful control over molecular motion in the future an extensive toolbox of both actionable molecules and stimuli-responsive units must be developed. Previously, our laboratory has reported 1,1′-disubstituted ferrocene (Fc) rotor units which assume a contracted/π-stacked conformation until complexation of cationic metal ions causes rotation about the Ferrocene (Fc) molecular ‘ball-bearing’. Herein, we explore the potential of using the photochemical ejection of [Ru(2,2′-bipyridyl)2]2+ units as a stimulus for the rotational contraction of new ferrocene rotor units. Fc rotors with both ‘regular’ and ‘inverse’ 2-pyridyl-1,2,3-triazole binding pockets and their corresponding [Ru(2,2′-bipyridyl)2]2+ complexes were synthesised. The rotors and complexes were characterised using nuclear magnetic resonance (NMR) and ultraviolet (UV)-visible spectroscopies, Electro-Spray Ionisation Mass Spectrometry (ESI–MS), and electrochemistry. The 1,1′-disubstituted Fc ligands were shown to π-stack both in solution and solid state. Density Functional Theory (DFT) calculations (CAM-B3LYP/6-31G(d)) support the notion that complexation to [Ru(2,2′-bipyridyl)2]2+ caused a rotation from the syn- to the anti-conformation. Upon photo-irradiation with UV light (254 nm), photo-ejection of the [Ru(2,2′-bipyridyl)2(CH3CN)2]2+ units in acetonitrile was observed. The re-complexation of the [Ru(2,2′-bipyridyl)2]2+ units could be achieved using acetone as the reaction solvent. However, the process was exceedingly slowly. Additionally, the Fc ligands slowly decomposed when exposed to UV irradiation meaning that only one extension and contraction cycle could be completed.

Feedback inhibition of actin on Rho mediates content release from large secretory vesicles

Secretion of adhesive glycoproteins to the lumen of Drosophila melanogaster larval salivary glands is performed by contraction of an actomyosin network assembled around large secretory vesicles, after their fusion to the apical membranes. We have identified a cycle of actin coat nucleation and disassembly that is independent of myosin. Recruitment of active Rho1 to the fused vesicle triggers activation of the formin Diaphanous and actin nucleation. This leads to actin-dependent localization of a RhoGAP protein that locally shuts off Rho1, promoting disassembly of the actin coat. When contraction of vesicles is blocked, the strict temporal order of the recruited elements generates repeated oscillations of actin coat formation and disassembly. Interestingly, different blocks to actin coat disassembly arrested vesicle contraction, indicating that actin turnover is an integral part of the actomyosin contraction cycle. The capacity of F-actin to trigger a negative feedback on its own production may be widely used to coordinate a succession of morphogenetic events or maintain homeostasis.

Formation and disassembly of a contractile actomyosin network mediates content release from large secretory vesicles

Secretion of adhesive glycoproteins to the lumen of Drosophila larval salivary glands is carried out by contraction of an actomyosin network that is assembled around large secretory vesicles, following their fusion to the apical membranes. We have identified a cycle of actin coat nucleation and disassembly that is independent of myosin. Recruitment of active Rho1 to the fused vesicle triggers activation of the formin Diaphanous and nucleation of linear actin. This, in turn, leads to actin-dependent localization of a RhoGAP protein that locally shuts off Rho1, promoting disassembly of the actin coat. Recruitment of the branched actin nucleation machinery is also required for effective Rho1 inactivation. Interestingly, different blocks to actin coat disassembly arrested vesicle contraction, indicating that actin turnover is an integral part of the actomyosin contraction cycle. The capacity of F-actin to trigger a negative feedback on its own production may be utilized in a variety of scenarios, to coordinate a succession of morphogenetic events or maintain homeostasis.SummaryThis work identified a cycle of actin assembly and disassembly in large secretory vesicles of Drosophila salivary glands. Actin disassembly is triggered by actin-dependent recruitment of a RhoGAP protein, and is essential for the contractility of the vesicle leading to content release to the lumen.