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.

A new bionic hydraulic actuator system for legged robots with impact buffering, impact energy absorption, impact energy storage, and force burst

It is a big challenge for bionic legged robots to realize desired jumping heights and forward-running speeds, let alone achieve springbok-style jump-running. A key limitation is that there is no actuator system that can mimic the springbok’s muscle system to drive leg–foot system movements. In this paper, we analyze the movement process of springboks and summarize some key characteristics of actuator systems. Some key concepts are then identified based on these key characteristics. Next, we propose a new bionic hydraulic joint actuator system with impact buffering, impact energy absorption, impact energy storage, and force burst, which can be applied to various legged robots to achieve higher running speeds, higher jumping heights, longer endurance, heavier loads, and lighter mass.

Muscle systems and motility of early animals highlighted by cnidarians from the basal Cambrian

Although fossil evidence suggest that various animal groups were able to move actively through their environment in the early stages of their evolution, virtually no direct information is available on the nature of their muscle systems. The origin of jellyfish swimming, for example, is of great concern to biologists. Exceptionally preserved muscles are described here in benthic peridermal olivooid medusozoans from the basal Cambrian of China (Kuanchuanpu Formation, ca. 535 Ma) that have direct equivalent in modern medusozoans. They consist of circular fibers distributed over the bell surface (subumbrella) and most probably have a myoepithelial origin. This is the oldest record of a muscle system in cnidarians and more generally in animals. This basic system was probably co-opted by younger early Cambrian jellyfish to develop capacities for the jet-propelled swimming within the water column. Additional lines of fossil evidence obtained from ecdysozoans (worms and panarthropods) show that the muscle systems of early animals underwent a rapid diversification through the early Cambrian and increased their capacity to colonize a wide range of habitats both within the water column and sediment at a critical time of their evolutionary radiation.

A Quantitative Proteomics Approach to Gain Insight into NRF2-KEAP1 Skeletal Muscle System and Its Cysteine Redox Regulation

Mammalian skeletal muscle (SkM) tissue engages the Nrf2-Keap1-dependent antioxidant defense mechanism to respond adaptively to stress. Redox homeostasis mediated by the reversible modification of selective cysteines is the prevalent mode of regulation. The protein targets of SkM redox regulation are largely unknown. We previously reported the proteomic profiles of soleus (Sol) and extensor digitorum longus (EDL) with Nrf2 or Keap1 gene deletion, using SkM-specific Nrf2 or Keap1 knockout models; iMS-Nrf2flox/flox; and iMS-Keap1flox/flox. Here, we employed these two animal models to understand the global expression profile of red tibialis anterior (RTA) using a label free approach and its redox proteomics using iodoacetyl tandem mass tag (iodoTMTTM)-labeled cysteine quantitation. We quantified 298 proteins that were significantly altered globally in the RTA with Nrf2 deficiency but only 21 proteins in the Keap1 KO samples. These proteins are involved in four intracellular signaling pathways: sirtuin signaling, Nrf2 mediated oxidative stress response, oxidative phosphorylation, and mitochondrion dysfunction. Moreover, we identified and quantified the cysteine redox peptides of 34 proteins, which are associated with mitochondrial oxidative phosphorylation, energy metabolism, and extracellular matrix. Our findings suggest that Nrf2-deficient RTA is implicated in metabolic myopathy, mitochondrial disorders, and motor dysfunction, possibly due to an enhanced oxidative modification of the structure and functional proteins in skeletal myocytes.

Systematic Transcriptome Analysis of Synovial Sarcoma Reveals Novel Transcriptional And Post-Transcriptional Abnormalities

Background: Synovial sarcoma (SS) is a rare and aggressive cancer that can come from distinct soft tissue types including muscle and ligaments. The SS transcriptome is crucial for understanding the SS biology; however, the transcriptomic landscape of SS is still poorly understood. Methods: We performed deep total RNA sequencing on ten paired SS and tumor-adjacent tissues to systematically dissect the transcriptomic profile of SS in terms of gene expression, alternative splicing, gene fusion, and circular RNAs.Results: A total of 2,309 upregulated and downregulated genes were identified between SS and tumor-adjacent tissues. Those upregulated genes could lead to the upregulation of the cell cycle, ribosome, and DNA replication pathways, while the downregulated genes may result in the downregulation of a set of metabolic biological processes and signaling pathways. Moreover, 2,511 genes (including 21 splicing factors) were differentially alternative spliced, indicating that the deregulation of alternative splicing could be one important factor that contributes to the tumorigenesis. Additionally, we identified the known gene fusions of SS18-SSX1/SSX2 as well as 11 potentially novel gene fusions. Interestingly, 49 circular RNAs were differentially expressed and their parental genes could function in muscle contraction and muscle system processes. Conclusions: Collectively, our comprehensive dissection of the transcriptomic profile of SS from both transcriptional and post-transcriptional levels provides novel insights into the biology and underlying molecular mechanism of SS.

The miR-133a, TPM4 and TAp63γ Role in Myocyte Differentiation Microfilament Remodelling and Colon Cancer Progression

MicroRNAs (miRNAs) play an essential role in the regulation of a number of physiological functions. miR-133a and other muscular miRs (myomiRs) play a key role in muscle cell growth and in some type of cancers. Here, we show that miR133a is upregulated in individuals that undertake physical exercise. We used a skeletal muscle differentiation model to dissect miR-133a’s role and to identify new targets, identifying Tropomyosin-4 (TPM4). This protein is expressed during muscle differentiation, but importantly it is an essential component of microfilament cytoskeleton and stress fibres formation. The microfilament scaffold remodelling is an essential step in cell transformation and tumour progression. Using the muscle system, we obtained valuable information about the microfilament proteins, and the knowledge on these molecular players can be transferred to the cytoskeleton rearrangement observed in cancer cells. Further investigations showed a role of TPM4 in cancer physiology, specifically, we found that miR-133a downregulation leads to TPM4 upregulation in colon carcinoma (CRC), and this correlates with a lower patient survival. At molecular level, we demonstrated in myocyte differentiation that TPM4 is positively regulated by the TA isoform of the p63 transcription factor. In muscles, miR-133a generates a myogenic stimulus, reducing the differentiation by downregulating TPM4. In this system, miR-133a counteracts the differentiative TAp63 activity. Interestingly, in CRC cell lines and in patient biopsies, miR-133a is able to regulate TPM4 activity, while TAp63 is not active. The downregulation of the miR leads to TPM4 overexpression, this modifies the architecture of the cell cytoskeleton contributing to increase the invasiveness of the tumour and associating with a poor prognosis. These results add data to the interesting question about the link between physical activity, muscle physiology and protection against colorectal cancer. The two phenomena have in common the cytoskeleton remodelling, due to the TPM4 activity, that is involved in stress fibres formation.

The Role of Extracellular Vesicles of Various Origins in the Development of Preeclampsia

Pre-eclampsia is a clinically unfavorable pregnancy outcome that determines the main indicators of maternal and/or perinatal morbidity and mortality. According to modern concepts, the placenta plays a central role in the development of PE, while intercellular and intervesicular communications involving extracellular vesicles (EVs, extracellular vesicles) initiate a cascade of various biological effects, determining the mechanisms of ontogenesis of the gestational process in normal and pathological conditions. Achievements in studies of extracellular vesicles (EVs, extracellular vesicles) are of particular interest both to clinicians and to researchers studying the pathophysiology of gestational complications. Extracellular vesicles (EVs) in preeclampsia are produced both by scintiotrophoblast and the maternal body - blood cells (platelets, red blood cells, white blood cells) and the cardiovascular (vascular endothelium, smooth muscle) system. Changes in the concentration of these EVs can contribute to the implementation of preeclampsia, enhancing the pro-inflammatory and procoagulant states inherent in the gestation process. This review focuses on freely available information on the possible interactions between placental and maternal EVs. Understanding the contribution of EVs to the development of preeclampsia can help to deepen knowledge about the pathogenesis of this pathology and determine the diagnostic and prognostic significance of extracellular vesicles as biomarkers.

Electrophysiological analysis of healthy and dystrophic 3D bioengineered skeletal muscle tissues

Recently, methods for creating three-dimensional (3D) human skeletal muscle tissues from myogenic cell lines have been reported. Bioengineered muscle tissues are contractile and respond to electrical and chemical stimulation. In this study we provide an electrophysiological analysis of healthy and dystrophic 3D bioengineered skeletal muscle tissues. We focus on Duchenne muscular dystrophy (DMD), a fatal muscle disorder involving the skeletal muscle system. The dystrophin gene, which when mutated causes DMD, encodes for the Dystrophin protein, which anchors the cytoskeletal network inside of a muscle cell to the extracellular matrix outside the cell. Here, we enlist a 3D in vitro model of DMD muscle tissue, to evaluate an understudied aspect of DMD, muscle cell electrical properties uncoupled from presynaptic neural inputs. Our data shows that electrophysiological aspects of DMD are replicated in the 3D bioengineered skeletal muscle tissue model. Furthermore, we test a block co-polymer, poloxamer 188, and demonstrate capacity for improving the membrane potential in DMD muscle. Therefore, this study serves as the baseline for a new in vitro method to examine potential therapies directed at muscular disorders.

Optimal Muscular Arrangement Using Genetic Algorithm for Musculoskeletal Potential Method with Muscle Viscosity

Muscle contractions (or equivalent mechanical elements) are responsible for joint movement in systems with musculoskeletal structure. Because muscles can only transmit force in the tensile direction in such systems, the internal force exists between the muscles. By utilizing the potential field generated by the internal force, the musculoskeletal potential method makes it possible to control the position without complex real-time calculations or sensory feedback by entering step-inputs of the balanced internal force at the target posture. However, the conditions of convergence to the target posture strongly depend on muscular arrangement. Previous studies have elucidated the mathematical conditions of the muscular arrangement; however, they provide sufficient conditions that must be satisfied by the muscular arrangement to converge to the target posture, which do not necessarily lead to optimal muscular arrangement conditions. This study proposes a method to determine the optimal muscular arrangement of a two-joint six-muscle system, wherein muscle viscosity is considered, that uses a genetic algorithm and an evaluation function considering the motion response time. The effect of the obtained muscular arrangement is verified in a simulation.