92 results about "Neuromuscular junction" patented technology

Apparatus for muscle activation, comprising: at least one electrode (138, 140, 142, 144) adapted to deliver a neuromuscular stimulation (NMES) signal to a body portion (146); at least one controller (124) adapted to provide a NMES signal comprising a sequence of stimulation signals to said at least one electrode; and a mechanical motion element (300) coupled to at least one of said body portion and a mirror body portion, wherein said mechanical motion element is operatively coupled to said at least one controller and wherein said at least one controller controls said NMES signal in conjunction with said mechanical motion element.

The present invention describes compositions and methods for treating, preventing and improving the appearance of skin, particularly, treating, preventing, ameliorating, reducing and/or eliminating fine lines and/or wrinkles of skin, wherein the compositions include limonoid constituents which inhibit acetylcholine release at neuromuscular junctions of skeletal muscle so as to relax the muscles involved with wrinkling, folding and creasing of skin, e.g., facial movement and expression. The limonoids preferably include the plant alkaloids toosendanin and azadirachtin. The compositions, which also are used to treat hyperhidrosis, are preferably applied to the skin, or are delivered by directed means to a site in need thereof.

A flexible sheet for neurostimulation is described having a flexible non-conductive substrate matrix in which electrodes are embedded along a lower surface. Electrically conductive wires extend from the electrodes through the flexible substrate to another exterior surface of the substrate. Methods of making the flexible sheet and making a device using the flexible sheet are also disclosed.

A system and method that provide a prophylactic treatment to a person, e.g., a patient, to avoid the occurrence of pulmonary embolisms by the system providing neuromuscular stimulation to a person's lower extremities, e.g., the person's legs, when the system senses that a person has been immobile for an extended period of time. An implantable neuromuscular pacer, such as that described in U.S. Pat. Nos. 5,193,539; 5,193,540; 6,164,284; 6,185,452; 6,208,894; 6,315,721; 6,564,807; and their progeny, may be used to provide to selectively provide such stimulation. Preferably, such a device may be battery powered so that it can operate independent of an external apparatus. In particular, systems and devices of the present invention preferably additionally include an activity monitor, e.g., an accelerometer or the like, that disables or limits stimulation to pronged time periods in which there is limited activity.

The invention provides compositions and methods for treating, preventing, and diagnosing diseases or conditions associated with an abnormal level or activity of biglycan; disorders associated with an unstable cytoplasmic membrane, due, e.g., to an unstable dystrophin associated protein complex (DAPC); disorders associated with abnormal synapses or neuromuscular junctions, including those resulting from an abnormal MuSK activation or acetylcholine receptor (AChR) aggregation. Examples of diseases include muscular dystrophies, such as Duchenne's Muscular Dystrophy, Becker's Muscular Dystrophy, neuromuscular disorders and neurological disorders.

Botulinum neurotoxins, the most potent of all toxins, induce lethal neuromuscular paralysis by inhibiting exocytosis at the neuromuscular junction. The light chains (LC) of these dichain neurotoxins are a new class of zinc-endopeptidases that specifically cleave the synaptosomal proteins, SNAP-25, VAMP, or syntaxin at discrete sites. The present invention relates to the construction, expression, purification, and use of synthetic or recombinant botulinum neutoroxin genes. For example, a synthetic gene for the LC of the botulinum neurotoxin serotype A (BoNT/A) was constructed and overexpressed in Escherichia coli. The gene product was purified from inclusion bodies. The methods of the invention can provide 1.1 g of the LC per liter of culture. The LC product was stable in solution at 4° C. for at least 6 months. This rBoNT/A LC was proteolytically active, specifically cleaving the Glu-Arg bond in a 17-residue synthetic peptide of SNAP-25, the reported cleavage site of BoNT/A. Its calculated catalytic efficiency k_cat/K_m was higher than that reported for the native BoNT/A dichain. Treating the rBoNT/A LC with mercuric compounds completely abolished its activity, most probably by modifying the cysteine-164 residue located in the vicinity of the active site. About 70% activity of the LC was restored by adding Zn²⁺ to a Zn²⁺-free, apo-LC preparation. The LC was nontoxic to mice and failed to elicit neutralizing epitope(s) when the animals were vaccinated with this protein. In addition, injecting rBoNT/A LC into sea urchin eggs inhibited exocytosis-dependent plasma membrane resealing.

The invention belongs to the field of biomedicine, and relates to a safe and reliable reprogrammed method for obtaining human iPS (induced pluripotent stem) cells, a method for simply, rapidly and efficiently inducing and differentiating iPS cells into spinal motoneurons, and a method for economically and efficiently obtaining functional spinal motoneurons and application of the method. Human fibroblasts are infected with Sendai virus carrying a reprogramming factor by using vitronectin as the sole growth medium, and are cultured for 3 weeks to obtain human iPS cells without exogenous serum interference; the iPS cells are efficiently induced and differentiated into spinal motoneurons by a combination of multiple small molecule compounds; and further, an astrocyte conditioned culture medium promotes maturation culture and is applied in the formation of neuromuscular junctions. The functional spinal motoneurons obtained by efficient induction can be applied to simulation of disease phenotype and discussion of pathogenesis, and provides a theoretical basis for the screening of effective therapeutic drugs in the future, and even in the future can be applied to the cell transplantation therapy of diseases.

A method for forming neuromuscular junctions includes forming functional neuromuscular junctions between motoneurons and muscle cells by co-culturing one or more human motoneurons and one or more rat muscle cells in a substantially serum-free medium. A synthetic mammalian neuromuscular junction includes a human motoneuron functionally linked to a rat muscle cell in a substantially serum-free medium. An artificial substrate may be used to support the one or more neuromuscular junctions.

Formulations of and dosing protocols for the administration of botulinum toxin that maximize efficacy and specificity while minimizing the likelihood of overdosing and undesirable side effects of treatment. The formulations include positively charged carriers, such as cationic peptides, which otherwise have no inherent botulinum-toxin-like activity. The dosing regimen is based on the pattern, quantity, and location of neuromuscular junctions in the target tissue. Because the number of neuromuscular junctions in a target tissue remains generally stable throughout life and because the pharmacological effect of botulinum toxin is localized at the neuromuscular junction, dosing efficacy is unaffected by muscle mass, age of the patient, or body weight.

The invention discloses a botanical pesticide, which consists of matrine, stemonine, nicotine, veratramine, osthole, chamaejasmine, root stem and leaf of hairypetal millettia, fulvic acid, an additive and a preservative. The botanical pesticide can paralyze feelers of pests to ensure that the feelers lose the function so as not to forage and mate, can also stimulate the skin of the pests at the same time to make sensory nerve of skin mucosa show an excitatory state to produce pruritus and burning heat sensation further to anaesthetize the pests so that the pests lose consciousness, and for the activity of neuromuscular junctions and nerve compound potential, stop the conduction of the excitement on nerve endings first, and can also make a nerve stem completely lose excitement and conduction impulse functions to die to ensure that the pests are also in a paralysis state even if the pests are not dead, lose the ability of damaging crops, and are nontoxic to human bodies at the same time.

The invention relates to culturing motor neuron cells together with skeletal muscle cells in a fluidic device under conditions whereby the interaction of these cells mimic the structure and function of the neuromuscular junction (NMJ) providing a NMJ-on-chip. Good viability, formation of myo-fibers and function of skeletal muscle cells on fluidic chips allow for measurements of muscle cell contractions. Embodiments of motor neurons co-cultures with contractile myo-fibers are contemplated for use with modeling diseases affecting NMJ's, e.g. Amyotrophic lateral sclerosis (ALS).