20 results about "Neuromuscular junction" patented technology

The invention provides a neuromuscular multi-element coupled organoid micro-fluidic chip, a device and a method. Relates to the technical field of organoid micro-fluidic chips. A first culture chamber, a second culture chamber and a third culture chamber are arranged in a culture layer of the chip; the first culture room is used for culturing nerve cells; the second culture room is used for culturing muscle cells; a microfluidic channel for communicating the first culture chamber with the second culture chamber is arranged between the first culture chamber and the second culture chamber; the third culture room is arranged on the micro-fluidic channel and is used for culturing a neuromuscular joint formed by convergence of axons of nerve cells and muscle cells; a microelectrode array plate is arranged in the circuit layer and is used for performing electrical stimulation and electrophysiological function detection on neuromuscular cells. Through the chip, co-culture of in-vitro nerves and muscle organs can be realized, a complex interaction relationship in a neuromuscular system can be accurately simulated, and the chip can also be used for constructing various neuromuscular related disease models.

The invention provides a motor neuron and myotubular cell co-culture method and model and application thereof. The motor neuron and myotubular cell co-culture method comprises the steps that motor neuron is cultured to form a neural network, and a motor neuron culture layer with the formed neural network is obtained; culturing myoblasts, inducing differentiation to form fine myotube cells, adding a mitosis inhibitor, and digesting and separating to obtain the fine myotube cells; and inoculating fine myotubular cells to the motor neuron culture layer with the formed neural network, and co-culturing. The co-culture method disclosed by the invention overcomes the limitation of a traditional nerve cell and muscle cell co-culture method, and has the advantages of simplicity, convenience, high efficiency, stability and the like. The method not only provides an effective experimental tool for related basic research of neuromuscular joint formation, physiological functions and the like, but also has wide application prospects in the fields of neuromuscular disease research, drug screening, toxicological research, gene therapy and the like.

In a method for inducing differentiation into neuromuscular junctions according to the present disclosure, the neuromuscular junctions are induced by: preculturing human pluripotent stem cells in a medium containing activin, bFGF, a WNT signal inhibitor, a BMP signal inhibitor, and a ROCK signal inhibitor; then culturing the stem cells in a medium containing bFGF, a ROCK signal inhibitor, a WNT signal activator, and a TGFβ signal inhibitor to differentiate into neuromesodermal cells; culturing the neuromesodermal cells in a medium containing a BMP signal inhibitor, a TGFβ signal inhibitor, a retinoic acid activator, and an SHH signal activator to differentiate into skeletal muscle progenitor cells and spinal motor neuron progenitor cells in the same culture dish; and culturing these progenitor cells in a medium for cell maturation containing BDNF, GDNF, AA, and dbcAMP.

A cell culture device and associated method for preparing an in vitro model of a neuromuscular junction (NMJ) is provided. The cell culture device has a cell culture layer (22) including a neuronal channel for receiving neuronal cells therein and a neuromuscular junction chamber in fluid communication with the neuronal channel for receiving muscle cells therein to allow co-culture of neuronal and muscle cells and form an NMJ. The neuronal channel includes a first portion having a first partial cross-section and a second portion downstream of the first portion for holding neuronal cells and having a second partial cross-section smaller than the first partial cross-section. The neuromuscular junction chamber can optionally include a support for culturing muscle cells therebetween. The in vitro model can be used, for example, to analyze biological material from a patient or to diagnose a condition.

This invention discloses a neuromuscular junction chip with force-induced structural color sensing and its fabrication method, belonging to the field of neuromuscular junction chip technology. It includes a substrate and a force-induced color-changing elastic structure. The substrate has a chamber for housing the neuromuscular junction. A first end of the force-induced color-changing elastic structure is fixedly connected to the substrate, and a second end of the structure can contact the muscle fiber bundles of the neuromuscular junction. When the muscle fiber bundles contract, they apply a force to the second end of the structure, causing it to elastically deform along a predetermined direction. The color of the structure changes as it deforms in this direction. This invention enables the visual characterization of the neuromuscular junction chip.

The present disclosure relates to anti-Muscle-Specific Kinase (MuSK) antibodies, in particular agonistic ant-MuSK antibodies, useful to restore or increase the function of the neuromuscular junction (NMJ).

The invention relates to the technical field of tennis training, in particular to a tennis core strength training model establishing method, which comprises the following steps of: inducing to generate muscle activation stimulation in a core muscle group through tennis training actions, and acquiring a total training stimulation amount based on a process that the muscle activation stimulation is captured by a muscle fiber and a nerve-muscle joint movement unit; determining a core strength increase equation based on the total training stimulation amount, and integrating the individual characteristic parameters of the athletes to construct a scalable core strength increase model; a scalable fatigue recovery model based on a BP neural network is obtained and used for quantifying the dynamic relation between the fatigue index and the athlete individual characteristics, training parameters and recovery time, and training cycle planning is optimized; a core strength increasing model and a fatigue recovery model are fused, a core strength training effect scalable model is formed, the change relation between the training effect and athlete individual characteristics, training parameters and training stages is comprehensively measured, and scientific and personalized core strength training scheme design and dynamic adjustment are achieved.

There are provided a cell culture device and associated method for preparing an in vitro model of a neuromuscular junction (NMJ). The cell culture device can include a cell culture layer that includes a neuronal cells channel for receiving neuronal cells therein, and a neuromuscular junction chamber in fluid communication with the neuronal cells channel to receive muscle cells therein to enable co-culture of the neuronal cells with the muscle cells and form the NMJ. The neuronal cells channel includes a first portion having a first portion cross-section and a second portion having a second portion cross-section that is smaller than the first portion cross-section and provided downstream of the first portion to retain neuronal cells. The neuromuscular junction chamber can optionally include pillars for culturing muscle cells therebetween. The in vitro model can be used for analysing a biological material from a patient or diagnose a condition, for instance.

This invention belongs to the field of veterinary drug technology. Specifically, it discloses a synergistic var. fluoraranil-moxicillin drop containing plant essential oils. The plant essential oils in the drop can disrupt the lipid structure of the parasite's epidermal wax layer, reduce the epidermal barrier function, increase epidermal permeability, and promote the rapid penetration of fluoraranil and moxicillin into the parasite, thereby increasing the drug concentration and shortening the onset time. At the same time, it also helps to enhance the effect of transdermal penetration enhancers. Fluoraranil acts on the parasite's GABA-gated chloride ion channels, moxicillin acts on the parasite's neuromuscular junction, and the plant essential oil exerts its insecticidal effect by disrupting the parasite's cell membrane integrity and inhibiting its metabolic enzyme activity. The three have different targets and no cross-resistance. They can synergistically block the key survival links of parasites, significantly improve the insecticidal rate, and delay the development of parasite resistance to single drugs.

Neuromuscular Monitoring A method of neuromuscular monitoring and corresponding apparatus for determining the effectiveness of a neuromuscular block. The method comprises inserting an electrode into a muscle of a mammalian subject, wherein the muscle has a singular branch of innervation, and the electrode extends to an innervation end point. The method is characterised by monitoring a sub-threshold potential at a neuromuscular junction of the muscle.

The present invention aims to provide an exercise assistance device that can effectively provide exercise assistance. [Solution] The exercise assist device of the present invention comprises at least an electrode group having a plurality of electrodes for detecting myoelectric potentials; an analysis means for analyzing and identifying the position of a neuromuscular junction in a muscle and the magnitude of the myoelectric potential at the neuromuscular junction based on a plurality of myoelectric potentials detected by the plurality of electrodes; a control means for generating a control signal corresponding to the magnitude of the myoelectric potential at the neuromuscular junction identified by the analysis means; an electrical stimulation generating means for generating an electrical stimulation controlled by the control means; and an electrical stimulation applying means for applying the electrical stimulation to the neuromuscular junction whose position has been identified by the analysis means. The electrode group is provided on the skin surface of at least two types of muscles, namely agonist muscles, antagonist muscles, and synergist muscles, and the electrical stimulation applying means is an electrode that has detected the myoelectric potential at the neuromuscular junction.

The present application relates to a method of promoting regeneration of neuromuscular junctions in a subject in need thereof. This method involves administering, to a subject in need thereof, a composition comprising a nucleic acid molecule encoding an AU-rich mRNA binding factor 1 (AUF1) protein or a functional fragment thereof under conditions effective to promote regeneration of neuromuscular junctions in the subject.

The present application relates to a method of promoting regeneration of neuromuscular junctions in a subject in need thereof. This method involves administering, to a subject in need thereof, a composition comprising a nucleic acid molecule encoding an AU-rich mRNA binding factor 1 (AUF1) protein or a functional fragment thereof under conditions effective to promote regeneration of neuromuscular junctions in the subject.

The present invention relates to a neurobiohybrid, a neuromuscular junction model using same, and a method for screening a drug related to motor neuron diseases using same. The present inventors have experimentally verified that the neurobiohybrid and the neuromuscular junction model using same of the present invention have an excellent effect on drug screening for treating amyotrophic lateral sclerosis (ALS), and thus the neurobiohybrid and the neuromuscular junction model using same are expected to be applicable to drug screening and toxicity evaluation for various neurological disorders.

The present disclosure relates to anti-Muscle-Specific Kinase (MuSK) antibodies, in particular agonistic ant-MuSK antibodies, useful to restore or increase the function of the neuromuscular junction (NMJ).

To provide a medicine for protecting and / or regenerating a neuromuscular junction, or an agent for protecting and / or regenerating a nervous system cell.SOLUTION: In one embodiment, the present invention provides an agent for protection and / or regeneration of a neuromuscular junction, or a therapeutic and / or prophylactic agent for a disease accompanied by a disorder of a neuromuscular junction, comprising an FF-MAS metabolism inhibitor. In addition, in one embodiment, the present invention provides a method for protecting and / or regenerating a neuromuscular junction, or a method for treating and / or preventing a disease associated with a disorder of neuromuscular junction, comprising administering an effective amount of FF-MAS metabolism inhibitor to a mammal. Further, in one aspect, the present invention provides an FF-MAS metabolism inhibitor for use in the protection and / or regeneration of a neuromuscular junction, or for use in the treatment and / or prevention of a disease associated with a disorder of a neuromuscular junction. In addition, in one aspect, the present invention provides use of an FF-MAS metabolism inhibitor for producing an agent for protecting and / or regenerating a neuromuscular junction, or for producing an agent for treating and / or preventing a disease associated with a disorder of a neuromuscular junction.SELECTED DRAWING: None

The invention is applicable to the technical field of biological medicines, and provides application of lisinopril in preparation of a medicine for treating amyotrophic lateral sclerosis. The invention has important value for promoting research and development of amyotrophic lateral sclerosis (ALS) treatment medicines and improving prognosis of patients. In-vitro experiments show that lisinopril can prevent mitochondria damage of NSC34 cells induced by SOD1G93A, expression of Beclin 1, LC3 and p62 is regulated by inhibiting a TGF [beta] 1 / PI3K / AKT / mTOR signal channel, cell autophagy is activated, and neuronal apoptosis is inhibited. In-vivo experiments show that lisinopril can activate in-vivo BI1 expression, regulate ALS model mouse lipid content and intervene in a glycerophospholipid metabolic process, and also can inhibit motor neuron death, myelin sheath shedding and neuromuscular junction degeneration and promote mitochondrial biogenesis by influencing autophagy regulated by a TGF [beta] 1 / PI3K / AKT / mTOR pathway.

The present invention relates to the field of medicine and cosmetology technology, and in particular to a cell active peptide composition with firming and anti-aging effects, and a preparation method and application thereof. The composition includes acetyl tetrapeptide-9, acetyl tetrapeptide-3, palmitoyl tetrapeptide-7, dipeptide-4, tripeptide-1, carnosine, snake venom peptide, acetyl hexapeptide-8, NAD+, ceramide, arnica flower extract, resveratrol, glutathione, dipeptide-1, panthenol, glabridin, and decarboxylated carnosine hydrochloride. The composition can activate cell energy; combat skin aging factors such as photoaging, reactive oxygen, inflammation, and saccharification; enhance skin barrier; promote extracellular matrix synthesis, strengthen basement membrane, and increase dermal density; strengthen subcutaneous adipose tissue; relax neuromuscular junctions, and smooth wrinkles. The composition is applied to skin medicine and cosmetology, reduces various wrinkles such as static lines and dynamic lines, improves the firmness and elasticity of the skin, and has multi-link firming and anti-aging effects such as wrinkle removal, lifting, and improvement of sagging.

Inhibition of glutamate-carboxypeptidase-II in and around the neuromuscular junctions (NMJ) of aged subjects can reduce age related reduction in muscle mass and strength. Compositions and methods for treating sarcopenia have been developed. Hydroxylated dendrimers conjugated with glutamate-carboxypeptidase-II (GCPII) inhibitors are administered in an amount effective to reduce, delay or reverse one or more symptoms or markers of sarcopenia. The hydroxylated dendrimer conjugated to a glutamate-carboxypeptidase-II (GCPII) inhibitor is in a dosage unit effective to reduce glutamate and / or increase NAAG within and / or around muscle macrophage and neuromuscular junctions (NMJ) in the subject.

Microfluidic devices with neuronal cells, muscle cells, and optionally other cell types co-cultured therein are provided. Typically one or more the cells has a mutation that contributes to or causes a neuronal or muscular disease or disorder. For example, in some embodiments, one or more of the cultured cells are derived from a subject with a neuronal or muscular disease or disorder. The microfluidic device can facilitate formation of a 3D motor unit and a neuromuscular junction in vitro, and be used to monitor the molecular, biochemical, cellular, and morphological differences in the formation of such structures by healthy and diseased cells, and for testing compounds, dosages of compounds, dosing regimes, and combinations thereof, that may improve or worsen their formation. An exemplary combination drug therapy identified in this way is also provided.