A fluid-driven soft robotic fish inspired by fish muscle architecture

Artificial fish-like robots developed to date often focus on the external morphology of fish and have rarely addressed the contribution of the structure and morphology of biological muscle. However, biological studies have proven that fish utilize the contraction of muscle fibers to drive the protective flexible connective tissue to swim. This paper introduces a pneumatic silicone structure prototype inspired by the red muscle system of fish and applies it to the fish-like robot named Flexi-Tuna. The key innovation is to make the fluid-driven units simulate the red muscle fiber bundles of fish and embed them into a flexible tuna-like matrix. The driving units act as muscle fibers to generate active contraction force, and the flexible matrix as connective tissue to generate passive deformation. Applying alternant pressure to the driving units can produce a bending moment, causing the tail to swing. As a result, the structural design of Flexi-Tuna has excellent bearing capacity compared with the traditional cavity-type and keeps the body smooth. On this basis, a general method is proposed for modeling the fish-like robot based on the independent analysis of the active and passive body, providing a foundation for Flexi-Tuna’s size design. Followed by the robot’s static and underwater dynamic tests, we used finite element static analysis and fluid numerical simulation to compare the results. The experimental results showed that the maximum swing angle of the tuna-like robot reached 20°, and the maximum thrust reached 0.185 N at the optimum frequency of 3.5 Hz. In this study, we designed a unique system that matches the functional level of biological muscles. As a result, we realized the application of fluid-driven artificial muscle to bionic fish and expanded new ideas for the structural design of flexible bionic fish.

Skeletal muscle regeneration is altered in the R6/2 mouse model of Huntington's disease

Huntington's disease (HD) is caused by CAG repeat expansion in the huntingtin (HTT) gene. Skeletal muscle wasting alongside central pathology is a well-recognized phenomenon seen in patients with HD and HD mouse models. HD muscle atrophy progresses with disease and affects prognosis and quality of life. Satellite cells, progenitors of mature skeletal muscle fibers, are essential for proliferation, differentiation, and repair of muscle tissue in response to muscle injury or exercise. In this study, we aim to investigate the effect of mutant HTT on the differentiation and regeneration capacity of HD muscle by employing in vitro mononuclear skeletal muscle cell isolation and in vivo acute muscle damage model in R6/2 mice. We found that, similar to R6/2 adult mice, neonatal R6/2 mice also exhibit a significant reduction in myofiber width and morphological changes in gastrocnemius and soleus muscles compared to WT mice. Cardiotoxin (CTX)-induced acute muscle damage in R6/2 and WT mice showed that the Pax7+ satellite cell pool was dampened in R6/2 mice at 4 weeks post-injection, and R6/2 mice exhibited an altered inflammatory profile in response to acute damage. Our results suggest that, in addition to the mutant HTT degenerative effects in mature muscle fibers, expression of mutant HTT in satellite cells might alter developmental and regenerative processes to contribute to the progressive muscle mass loss in HD. Taken together, the results presented here encourage further studies evaluating the underlying mechanisms of satellite cell dysfunction in HD mouse models.

Microstructural Dynamics of the Myocardium: Orientation of the Muscle Fibers and Occurrence of Cardiomyopathies

This paper considers the Holzapfel–Ogden (HO) model to examine the behavior of the left ventricle myocardium. At the tissue level, we analyze the contributions of the orientation angle of muscle fibers (MFs) and investigate their effects on the occurrence of certain cardiomyopathies and congenital diseases at the organ level. Knowing the importance of myocardial microstructure on cardiac function, we vary the angle between the direction of collagen sheets and MFs in all layers of the myocardium (from epicardium to endocardium) to model the effects of tilted MFs. Based on the HO model in which the directions of the fibers are orthogonal and using the strain energy of HO, we construct a tensile-compression test and simulate the dynamics of a cubic sample. We recover the authors’ results exhibiting the existence of residual stresses in various directions. Then, we modify the energy of HO slightly to assess the impact of the same stress states on the system with tilted MFs. A numerical tensile-compression test performed on this new cubic sample shows that, in certain directions, the heart tissue is more resistant to shear deformations in some planes than in others. Moreover, it appears that the residual stress is smaller as the angle of orientation of the MFs is small. Furthermore, we observe that the residual stress is greater in the new model compared to the normal HO model. This could affect the heart muscle at the organ level leading to hypertrophied/dilated cardiomyopathy.

Targeting necroptosis in muscle fibers ameliorates inflammatory myopathies

Muscle cell death in polymyositis is induced by CD8+ cytotoxic T lymphocytes. We hypothesized that the injured muscle fibers release pro-inflammatory molecules, which would further accelerate CD8+ cytotoxic T lymphocytes-induced muscle injury, and inhibition of the cell death of muscle fibers could be a novel therapeutic strategy to suppress both muscle injury and inflammation in polymyositis. Here, we show that the pattern of cell death of muscle fibers in polymyositis is FAS ligand-dependent necroptosis, while that of satellite cells and myoblasts is perforin 1/granzyme B-dependent apoptosis, using human muscle biopsy specimens of polymyositis patients and models of polymyositis in vitro and in vivo. Inhibition of necroptosis suppresses not only CD8+ cytotoxic T lymphocytes-induced cell death of myotubes but also the release of inflammatory molecules including HMGB1. Treatment with a necroptosis inhibitor or anti-HMGB1 antibodies ameliorates myositis-induced muscle weakness as well as muscle cell death and inflammation in the muscles. Thus, targeting necroptosis in muscle cells is a promising strategy for treating polymyositis providing an alternative to current therapies directed at leukocytes.

Dynamics of morphological and immunohistochemical changes in myocardium during hypothyroidism modeling in experiment

An experimental model of hypothyroidism was obtained by thyroidectomy. The operation was carried out on 57 sexually mature male rats weighing 250–300 g. The experiment lasted 45 days. Laboratory animals were removed from the experiment on days 7th, 14th, 21st, 28th, 35th and 45th. As a control, 15 rats were used that were not operated on. For histological examination, pieces of rat myocardium were taken from the left and right ventricles. The pieces were fixed in 10% buffered formalin for 10 days. Histological sections were prepared in a standard manner. Sections were stained with hematoxylin and eosin, picrofuchsin according to van Gieson, toluidine blue, according to Mallory. Results of the study: In the myocardium of rats, hemodynamic disorders, edema, hydropic degeneration of cardiomyocytes, myocytolysis, fragmentation of muscle fibers, colliquation necrosis, compression and atrophy of muscle fibers were found. An immunohistochemical study revealed a decrease in the expression of desmin and sarcomeric actin.

Evaluation of Cardiovascular Experiment Animal

In vivo models of myocardial infarction induced by coronary artery ligation in rats usually suffer from high early mortality and a low rate of induction. This study investigated the time course initiation of chronic myocardial infarction in albino rats and the possibility of reducing early mortality rate due to myocardial infarction by modification of the surgical technique. CAL was carried out by passing the suture through the pericardial layer around the midway of the left anterior descending coronary artery including a small area of the myocardium to avoid mechanical damage to the heart geometry. In addition, the role of endothelin-1 in rat heart with congestive heart failure was critically assessed. Time course initiation experiments were designed by sacrificing the animals at different time intervals and by carrying out physiological, biochemical, histopathological, electron microscopical and immunohistochemical studies. Specific markers of myocardial injury, viz. cardiac troponin-T, high sensitivity C-reactive protein, lactate dehydrogenase and fibrinogen were measured at different time points. Serum marker enzymes and activities of lysosomal hydrolases were found to be elevated on the eighth day post-ligation. Histopathological studies demonstrated focal areas showing fibrovascular tissue containing fibroblasts, collagenous ground substance and numerous small capillaries replacing cardiac muscle fibers. Transmission electron micrographs exhibited mitochondrial changes of well-developed irreversible cardiac injury, viz. swelling, disorganization of cristae, appearance of mitochondrial amorphous matrix densities, and significant distortion of muscle fibers and distinct disruption of the intercalated discs. Immune blotting studies confirmed the presence of alpha 2-macroglobulin which supported the inflammatory response. The severity of the CMI was inferred by the measurement of the level of ET-1 in plasma and left ventricle which was significantly higher in the CMI rats than in the sham-operated rats. Immunohistochemical studies at different time intervals showed that there was a significant immunoexpression of ET-1 on the eighth day post-ligation. This study conclusively showed that ligation of left anterior descending artery minimised mortality and ET-1 was expressed during CMI.

Histomorphometric study of the soleus muscle under conditions of modeling of spinal cord contusion injury: experimental morphological study

Objective. To conduct a morphometric analysis of the soleus muscle of rats after moderate spinal cord contusion injury.Material and Methods. Experiments were performed on female Wistar rats aged 8–12 months, weighing 270–320 g. Animals of the experimental group (n = 25) underwent laminectomy at the T9 level under general anesthesia and modeling of spinal contusion injury of moderate severity. Intact rats constituted the control group (n = 10). Euthanasia was performed on the 5th, 15th, 30th, 60th, 90th, and 180th days of the experiment. Paraffin sections were stained with hematoxylin-eosin and Masson, the diameters of muscle fibers were determined by computer morphometry, and histograms of their distribution were obtained.Results. In the soleus muscle, the signs of reversible reparative processes prevailed in response to neurotrophic damage. It was evidenced by a local increase in the diversity of myocyte diameters and the loss of polygonality of their profiles, focal destruction of muscle fibers, activation of the connective tissue component, disorganization of some intramuscular nerve conductors, and vascular fibrosis of perimysium. Nevertheless, the histostructure of an intact muscle prevailed in the course of the experiment, which was confirmed by the data of morphometric analysis. All histograms of the distribution of the muscle fiber diameters are unimodal with a mode in the range of 30–41 μm. On the 180th day, the maximum myocyte diameters in the histogram of the left limb muscle belonged to the range of 21–30 μm, which was typical for histograms in the intact group.Conclusion. The nature of the plastic reorganization of the soleus muscle when neurotrophic control is impaired indicates compensatory regeneration of muscle tissue by the type of restitution, which opens up the possibility of predicting the rehabilitation period. It is advisable to take this into account when developing medical and social programs and therapeutic measures, where the most important role is played by superficial neuromuscular and functional electrical stimulation.