13 results about "Neuromuscular junction" patented technology

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.

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 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.