Botulinum Toxins, Type A: A serotype of botulinum toxins that has specificity for cleavage of SYNAPTOSOMAL-ASSOCIATED PROTEIN 25.Botulinum Toxins: Toxic proteins produced from the species CLOSTRIDIUM BOTULINUM. The toxins are synthesized as a single peptide chain which is processed into a mature protein consisting of a heavy chain and light chain joined via a disulfide bond. The botulinum toxin light chain is a zinc-dependent protease which is released from the heavy chain upon ENDOCYTOSIS into PRESYNAPTIC NERVE ENDINGS. Once inside the cell the botulinum toxin light chain cleaves specific SNARE proteins which are essential for secretion of ACETYLCHOLINE by SYNAPTIC VESICLES. This inhibition of acetylcholine release results in muscular PARALYSIS.Neuromuscular Agents: Drugs used for their actions on skeletal muscle. Included are agents that act directly on skeletal muscle, those that alter neuromuscular transmission (NEUROMUSCULAR BLOCKING AGENTS), and drugs that act centrally as skeletal muscle relaxants (MUSCLE RELAXANTS, CENTRAL). Drugs used in the treatment of movement disorders are ANTI-DYSKINESIA AGENTS.Clostridium botulinum: A species of anaerobic, gram-positive, rod-shaped bacteria in the family Clostridiaceae that produces proteins with characteristic neurotoxicity. It is the etiologic agent of BOTULISM in humans, wild fowl, HORSES; and CATTLE. Seven subtypes (sometimes called antigenic types, or strains) exist, each producing a different botulinum toxin (BOTULINUM TOXINS). The organism and its spores are widely distributed in nature.Anti-Dyskinesia Agents: Drugs used in the treatment of movement disorders. Most of these act centrally on dopaminergic or cholinergic systems. Among the most important clinically are those used for the treatment of Parkinson disease (ANTIPARKINSON AGENTS) and those for the tardive dyskinesias.Botulism: A disease caused by potent protein NEUROTOXINS produced by CLOSTRIDIUM BOTULINUM which interfere with the presynaptic release of ACETYLCHOLINE at the NEUROMUSCULAR JUNCTION. Clinical features include abdominal pain, vomiting, acute PARALYSIS (including respiratory paralysis), blurred vision, and DIPLOPIA. Botulism may be classified into several subtypes (e.g., food-borne, infant, wound, and others). (From Adams et al., Principles of Neurology, 6th ed, p1208)Botulinum Antitoxin: Antiserum given therapeutically in BOTULISM.Blepharospasm: Excessive winking; tonic or clonic spasm of the orbicularis oculi muscle.Spasm: An involuntary contraction of a muscle or group of muscles. Spasms may involve SKELETAL MUSCLE or SMOOTH MUSCLE.Muscle Spasticity: A form of muscle hypertonia associated with upper MOTOR NEURON DISEASE. Resistance to passive stretch of a spastic muscle results in minimal initial resistance (a "free interval") followed by an incremental increase in muscle tone. Tone increases in proportion to the velocity of stretch. Spasticity is usually accompanied by HYPERREFLEXIA and variable degrees of MUSCLE WEAKNESS. (From Adams et al., Principles of Neurology, 6th ed, p54)Injections, Intramuscular: Forceful administration into a muscle of liquid medication, nutrient, or other fluid through a hollow needle piercing the muscle and any tissue covering it.Torticollis: A symptom, not a disease, of a twisted neck. In most instances, the head is tipped toward one side and the chin rotated toward the other. The involuntary muscle contractions in the neck region of patients with torticollis can be due to congenital defects, trauma, inflammation, tumors, and neurological or other factors.Sialorrhea: Increased salivary flow.Tetanus Toxin: Protein synthesized by CLOSTRIDIUM TETANI as a single chain of ~150 kDa with 35% sequence identity to BOTULINUM TOXIN that is cleaved to a light and a heavy chain that are linked by a single disulfide bond. Tetanolysin is the hemolytic and tetanospasmin is the neurotoxic principle. The toxin causes disruption of the inhibitory mechanisms of the CNS, thus permitting uncontrolled nervous activity, leading to fatal CONVULSIONS.Fissure in Ano: A painful linear ulcer at the margin of the anus. It appears as a crack or slit in the mucous membrane of the anus and is very painful and difficult to heal. (Dorland, 27th ed & Stedman, 25th ed)Meige Syndrome: A syndrome characterized by orofacial DYSTONIA; including BLEPHAROSPASM; forceful jaw opening; lip retraction; platysma muscle spasm; and tongue protrusion. It primarily affects older adults, with an incidence peak in the seventh decade of life. (From Adams et al., Principles of Neurology, 6th ed, p108)Clostridium botulinum type A: Subtype of CLOSTRIDIUM BOTULINUM that produces BOTULINUM TOXINS, TYPE A which is neurotoxic to humans and animals.Clostridium botulinum type E: Subtype of CLOSTRIDIUM BOTULINUM that produces botulinum toxin type E which is neurotoxic to humans and animals.Cholera Toxin: An ENTEROTOXIN from VIBRIO CHOLERAE. It consists of two major protomers, the heavy (H) or A subunit and the B protomer which consists of 5 light (L) or B subunits. The catalytic A subunit is proteolytically cleaved into fragments A1 and A2. The A1 fragment is a MONO(ADP-RIBOSE) TRANSFERASE. The B protomer binds cholera toxin to intestinal epithelial cells, and facilitates the uptake of the A1 fragment. The A1 catalyzed transfer of ADP-RIBOSE to the alpha subunits of heterotrimeric G PROTEINS activates the production of CYCLIC AMP. Increased levels of cyclic AMP are thought to modulate release of fluid and electrolytes from intestinal crypt cells.Hyperhidrosis: Excessive sweating. In the localized type, the most frequent sites are the palms, soles, axillae, inguinal folds, and the perineal area. Its chief cause is thought to be emotional. Generalized hyperhidrosis may be induced by a hot, humid environment, by fever, or by vigorous exercise.Injections: Introduction of substances into the body using a needle and syringe.Neurotoxins: Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept.Dystonia: An attitude or posture due to the co-contraction of agonists and antagonist muscles in one region of the body. It most often affects the large axial muscles of the trunk and limb girdles. Conditions which feature persistent or recurrent episodes of dystonia as a primary manifestation of disease are referred to as DYSTONIC DISORDERS. (Adams et al., Principles of Neurology, 6th ed, p77)Hemifacial Spasm: Recurrent clonic contraction of facial muscles, restricted to one side. It may occur as a manifestation of compressive lesions involving the seventh cranial nerve (FACIAL NERVE DISEASES), during recovery from BELL PALSY, or in association with other disorders. (From Adams et al., Principles of Neurology, 6th ed, p1378)Esophageal Achalasia: A motility disorder of the ESOPHAGUS in which the LOWER ESOPHAGEAL SPHINCTER (near the CARDIA) fails to relax resulting in functional obstruction of the esophagus, and DYSPHAGIA. Achalasia is characterized by a grossly contorted and dilated esophagus (megaesophagus).Facial Muscles: Muscles of facial expression or mimetic muscles that include the numerous muscles supplied by the facial nerve that are attached to and move the skin of the face. (From Stedman, 25th ed)Dystonic Disorders: Acquired and inherited conditions that feature DYSTONIA as a primary manifestation of disease. These disorders are generally divided into generalized dystonias (e.g., dystonia musculorum deformans) and focal dystonias (e.g., writer's cramp). They are also classified by patterns of inheritance and by age of onset.T-2 Toxin: A potent mycotoxin produced in feedstuffs by several species of the genus FUSARIUM. It elicits a severe inflammatory reaction in animals and has teratogenic effects.Sweating, Gustatory: An autonomic disorder characterized by excessive sweating of the forehead, upper lip, perioral region, or sternum subsequent to gustatory stimuli. The auriculotemporal syndrome features facial flushing or sweating limited to the distribution of the auriculotemporal nerve and may develop after trauma to the parotid gland, in association with PAROTID NEOPLASMS, or following their surgical removal. (From Ann Neurol 1997 Dec;42(6):973-5)Synaptosomal-Associated Protein 25: A ubiquitous target SNARE protein that interacts with SYNTAXIN and SYNAPTOBREVIN. It is a core component of the machinery for intracellular MEMBRANE FUSION. The sequence contains 2 SNARE domains, one is the prototype for the Qb-SNARES, and the other is the prototype for the Qc-SNARES.Cerebral Palsy: A heterogeneous group of nonprogressive motor disorders caused by chronic brain injuries that originate in the prenatal period, perinatal period, or first few years of life. The four major subtypes are spastic, athetoid, ataxic, and mixed cerebral palsy, with spastic forms being the most common. The motor disorder may range from difficulties with fine motor control to severe spasticity (see MUSCLE SPASTICITY) in all limbs. Spastic diplegia (Little disease) is the most common subtype, and is characterized by spasticity that is more prominent in the legs than in the arms. Pathologically, this condition may be associated with LEUKOMALACIA, PERIVENTRICULAR. (From Dev Med Child Neurol 1998 Aug;40(8):520-7)Toxins, Biological: Specific, characterizable, poisonous chemicals, often PROTEINS, with specific biological properties, including immunogenicity, produced by microbes, higher plants (PLANTS, TOXIC), or ANIMALS.Antitoxins: Antisera from immunized animals that is purified and used as a passive immunizing agent against specific BACTERIAL TOXINS.Oculomotor Muscles: The muscles that move the eye. Included in this group are the medial rectus, lateral rectus, superior rectus, inferior rectus, inferior oblique, superior oblique, musculus orbitalis, and levator palpebrae superioris.Urinary Bladder, Overactive: Symptom of overactive detrusor muscle of the URINARY BLADDER that contracts with abnormally high frequency and urgency. Overactive bladder is characterized by the frequent feeling of needing to urinate during the day, during the night, or both. URINARY INCONTINENCE may or may not be present.Equinus Deformity: Plantar declination of the foot.Clostridium botulinum type B: Subtype of CLOSTRIDIUM BOTULINUM that produces botulinum toxin type B which is neurotoxic to humans and animals.Rejuvenation: The phenomenon of youthfulness, vitality, and freshness being restored. This can apply to appearance, TISSUES, organ functions, or other areas.Skin Aging: The process of aging due to changes in the structure and elasticity of the skin over time. It may be a part of physiological aging or it may be due to the effects of ultraviolet radiation, usually through exposure to sunlight.Cosmetic Techniques: Procedures for the improvement or enhancement of the appearance of the visible parts of the body.Toxoids: Preparations of pathogenic organisms or their derivatives made nontoxic and intended for active immunologic prophylaxis. They include deactivated toxins. Anatoxin toxoids are distinct from anatoxins that are TROPANES found in CYANOBACTERIA.Clostridium botulinum type F: Subtype of CLOSTRIDIUM BOTULINUM that produces botulinum toxin type F which is neurotoxic to humans and animals.Neuromuscular Junction: The synapse between a neuron and a muscle.Treatment Outcome: Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.Paralysis: A general term most often used to describe severe or complete loss of muscle strength due to motor system disease from the level of the cerebral cortex to the muscle fiber. This term may also occasionally refer to a loss of sensory function. (From Adams et al., Principles of Neurology, 6th ed, p45)Clostridium botulinum type D: Subtype of CLOSTRIDIUM BOTULINUM that produces botulinum toxin type D which is neurotoxic to ANIMALS, especially CATTLE, but not humans.Neuromuscular Blocking Agents: Drugs that interrupt transmission of nerve impulses at the skeletal neuromuscular junction. They can be of two types, competitive, stabilizing blockers (NEUROMUSCULAR NONDEPOLARIZING AGENTS) or noncompetitive, depolarizing agents (NEUROMUSCULAR DEPOLARIZING AGENTS). Both prevent acetylcholine from triggering the muscle contraction and they are used as anesthesia adjuvants, as relaxants during electroshock, in convulsive states, etc.Injections, Intralesional: Injections introduced directly into localized lesions.Marine Toxins: Toxic or poisonous substances elaborated by marine flora or fauna. They include also specific, characterized poisons or toxins for which there is no more specific heading, like those from poisonous FISHES.Lethal Dose 50: The dose amount of poisonous or toxic substance or dose of ionizing radiation required to kill 50% of the tested population.R-SNARE Proteins: SNARE proteins where the central amino acid residue of the SNARE motif is an ARGININE. They are classified separately from the Q-SNARE PROTEINS where the central amino acid residue of the SNARE motif is a GLUTAMINE. This subfamily contains the vesicle associated membrane proteins (VAMPs) based on similarity to the prototype for the R-SNAREs, VAMP2 (synaptobrevin 2).ADP Ribose Transferases: Enzymes that transfer the ADP-RIBOSE group of NAD or NADP to proteins or other small molecules. Transfer of ADP-ribose to water (i.e., hydrolysis) is catalyzed by the NADASES. The mono(ADP-ribose)transferases transfer a single ADP-ribose. POLY(ADP-RIBOSE) POLYMERASES transfer multiple units of ADP-ribose to protein targets, building POLY ADENOSINE DIPHOSPHATE RIBOSE in linear or branched chains.Manometry: Measurement of the pressure or tension of liquids or gases with a manometer.Voice Disorders: Pathological processes that affect voice production, usually involving VOCAL CORDS and the LARYNGEAL MUCOSA. Voice disorders can be caused by organic (anatomical), or functional (emotional or psychological) factors leading to DYSPHONIA; APHONIA; and defects in VOICE QUALITY, loudness, and pitch.Food Microbiology: The presence of bacteria, viruses, and fungi in food and food products. This term is not restricted to pathogenic organisms: the presence of various non-pathogenic bacteria and fungi in cheeses and wines, for example, is included in this concept.Melia: A plant genus of the family MELIACEAE. Members contain meliavolkinin, melianin C and limonoids.Sphincter of Oddi: The sphincter of the hepatopancreatic ampulla within the duodenal papilla. The COMMON BILE DUCT and main pancreatic duct pass through this sphincter.Hemiplegia: Severe or complete loss of motor function on one side of the body. This condition is usually caused by BRAIN DISEASES that are localized to the cerebral hemisphere opposite to the side of weakness. Less frequently, BRAIN STEM lesions; cervical SPINAL CORD DISEASES; PERIPHERAL NERVOUS SYSTEM DISEASES; and other conditions may manifest as hemiplegia. The term hemiparesis (see PARESIS) refers to mild to moderate weakness involving one side of the body.Shiga Toxins: A class of toxins that inhibit protein synthesis by blocking the interaction of ribosomal RNA; (RNA, RIBOSOMAL) with PEPTIDE ELONGATION FACTORS. They include SHIGA TOXIN which is produced by SHIGELLA DYSENTERIAE and a variety of shiga-like toxins that are produced by pathologic strains of ESCHERICHIA COLI such as ESCHERICHIA COLI O157.Muscle Hypertonia: Abnormal increase in skeletal or smooth muscle tone. Skeletal muscle hypertonicity may be associated with PYRAMIDAL TRACT lesions or BASAL GANGLIA DISEASES.Synkinesis: An involuntary movement accompanying a volitional movement. It often refers to facial movements that accompany FACIAL PARALYSIS.Strabismus: Misalignment of the visual axes of the eyes. In comitant strabismus the degree of ocular misalignment does not vary with the direction of gaze. In noncomitant strabismus the degree of misalignment varies depending on direction of gaze or which eye is fixating on the target. (Miller, Walsh & Hoyt's Clinical Neuro-Ophthalmology, 4th ed, p641)Facial Nerve: The 7th cranial nerve. The facial nerve has two parts, the larger motor root which may be called the facial nerve proper, and the smaller intermediate or sensory root. Together they provide efferent innervation to the muscles of facial expression and to the lacrimal and SALIVARY GLANDS, and convey afferent information for TASTE from the anterior two-thirds of the TONGUE and for TOUCH from the EXTERNAL EAR.Upper Extremity: The region of the upper limb in animals, extending from the deltoid region to the HAND, and including the ARM; AXILLA; and SHOULDER.Injections, Intradermal: The forcing into the skin of liquid medication, nutrient, or other fluid through a hollow needle, piercing the top skin layer.Muscle Denervation: The resection or removal of the innervation of a muscle or muscle tissue.Gastroparesis: Chronic delayed gastric emptying. Gastroparesis may be caused by motor dysfunction or paralysis of STOMACH muscles or may be associated with other systemic diseases such as DIABETES MELLITUS.Shiga Toxin 2: A toxin produced by certain pathogenic strains of ESCHERICHIA COLI such as ESCHERICHIA COLI O157. It shares 50-60% homology with SHIGA TOXIN and SHIGA TOXIN 1.Cholinergic Antagonists: Drugs that bind to but do not activate CHOLINERGIC RECEPTORS, thereby blocking the actions of ACETYLCHOLINE or cholinergic agonists.Muscle Relaxants, Central: A heterogeneous group of drugs used to produce muscle relaxation, excepting the neuromuscular blocking agents. They have their primary clinical and therapeutic uses in the treatment of muscle spasm and immobility associated with strains, sprains, and injuries of the back and, to a lesser degree, injuries to the neck. They have been used also for the treatment of a variety of clinical conditions that have in common only the presence of skeletal muscle hyperactivity, for example, the muscle spasms that can occur in MULTIPLE SCLEROSIS. (From Smith and Reynard, Textbook of Pharmacology, 1991, p358)Adenosine Diphosphate Ribose: An ester formed between the aldehydic carbon of RIBOSE and the terminal phosphate of ADENOSINE DIPHOSPHATE. It is produced by the hydrolysis of nicotinamide-adenine dinucleotide (NAD) by a variety of enzymes, some of which transfer an ADP-ribosyl group to target proteins.Biological Assay: A method of measuring the effects of a biologically active substance using an intermediate in vivo or in vitro tissue or cell model under controlled conditions. It includes virulence studies in animal fetuses in utero, mouse convulsion bioassay of insulin, quantitation of tumor-initiator systems in mouse skin, calculation of potentiating effects of a hormonal factor in an isolated strip of contracting stomach muscle, etc.HandwritingClostridium: A genus of motile or nonmotile gram-positive bacteria of the family Clostridiaceae. Many species have been identified with some being pathogenic. They occur in water, soil, and in the intestinal tract of humans and lower animals.Neck Muscles: The neck muscles consist of the platysma, splenius cervicis, sternocleidomastoid(eus), longus colli, the anterior, medius, and posterior scalenes, digastric(us), stylohyoid(eus), mylohyoid(eus), geniohyoid(eus), sternohyoid(eus), omohyoid(eus), sternothyroid(eus), and thyrohyoid(eus).Shiga Toxin 1: A toxin produced by certain pathogenic strains of ESCHERICHIA COLI such as ESCHERICHIA COLI O157. It is closely related to SHIGA TOXIN produced by SHIGELLA DYSENTERIAE.Electromyography: Recording of the changes in electric potential of muscle by means of surface or needle electrodes.Eyelid DiseasesFacial Paralysis: Severe or complete loss of facial muscle motor function. This condition may result from central or peripheral lesions. Damage to CNS motor pathways from the cerebral cortex to the facial nuclei in the pons leads to facial weakness that generally spares the forehead muscles. FACIAL NERVE DISEASES generally results in generalized hemifacial weakness. NEUROMUSCULAR JUNCTION DISEASES and MUSCULAR DISEASES may also cause facial paralysis or paresis.Arthropod Venoms: Venoms from animals of the phylum Arthropoda. Those most investigated are from scorpions and spiders of the class Arachnidae and from ant, bee, and wasp families of the Insecta order Hymenoptera. The venoms contain protein toxins, enzymes, and other bioactive substances and may be lethal to man.Sweat Glands: Sweat-producing structures that are embedded in the DERMIS. Each gland consists of a single tube, a coiled body, and a superficial duct.Fish Products: Food products manufactured from fish (e.g., FISH FLOUR, fish meal).Paraparesis, Spastic: Mild or moderate loss of motor function accompanied by spasticity in the lower extremities. This condition is a manifestation of CENTRAL NERVOUS SYSTEM DISEASES that cause injury to the motor cortex or descending motor pathways.Laryngeal Muscles: The striated muscle groups which move the LARYNX as a whole or its parts, such as altering tension of the VOCAL CORDS, or size of the slit (RIMA GLOTTIDIS).Ophthalmoplegia: Paralysis of one or more of the ocular muscles due to disorders of the eye muscles, neuromuscular junction, supporting soft tissue, tendons, or innervation to the muscles.Exocytosis: Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the CELL MEMBRANE.Urinary Bladder, Neurogenic: Dysfunction of the URINARY BLADDER due to disease of the central or peripheral nervous system pathways involved in the control of URINATION. This is often associated with SPINAL CORD DISEASES, but may also be caused by BRAIN DISEASES or PERIPHERAL NERVE DISEASES.Esotropia: A form of ocular misalignment characterized by an excessive convergence of the visual axes, resulting in a "cross-eye" appearance. An example of this condition occurs when paralysis of the lateral rectus muscle causes an abnormal inward deviation of one eye on attempted gaze.Double-Blind Method: A method of studying a drug or procedure in which both the subjects and investigators are kept unaware of who is actually getting which specific treatment.Food Preservation: Procedures or techniques used to keep food from spoiling.Dysphonia: Difficulty and/or pain in PHONATION or speaking.rhoB GTP-Binding Protein: A GTP-BINDING PROTEIN involved in regulating a signal transduction pathway that controls assembly of focal adhesions and actin stress fibers. This enzyme was formerly listed as EC 3.6.1.47.Splints: Rigid or flexible appliances used to maintain in position a displaced or movable part or to keep in place and protect an injured part. (Dorland, 28th ed)Biological Warfare: Warfare involving the use of living organisms or their products as disease etiologic agents against people, animals, or plants.Eyelids: Each of the upper and lower folds of SKIN which cover the EYE when closed.Esophageal Spasm, Diffuse: A hypermotility disorder of the ESOPHAGUS that is characterized by spastic non-peristaltic responses to SWALLOWING; CHEST PAIN; and DYSPHAGIA.Pain Measurement: Scales, questionnaires, tests, and other methods used to assess pain severity and duration in patients or experimental animals to aid in diagnosis, therapy, and physiological studies.Urodynamics: The mechanical laws of fluid dynamics as they apply to urine transport.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Dyskinesias: Abnormal involuntary movements which primarily affect the extremities, trunk, or jaw that occur as a manifestation of an underlying disease process. Conditions which feature recurrent or persistent episodes of dyskinesia as a primary manifestation of disease may be referred to as dyskinesia syndromes (see MOVEMENT DISORDERS). Dyskinesias are also a relatively common manifestation of BASAL GANGLIA DISEASES.Enterotoxins: Substances that are toxic to the intestinal tract causing vomiting, diarrhea, etc.; most common enterotoxins are produced by bacteria.Motor Endplate: The specialized postsynaptic region of a muscle cell. The motor endplate is immediately across the synaptic cleft from the presynaptic axon terminal. Among its anatomical specializations are junctional folds which harbor a high density of cholinergic receptors.Clostridium botulinum type C: Subtype of CLOSTRIDIUM BOTULINUM that produces botulinum toxin type C which is neurotoxic to ANIMALS, especially CATTLE, but not humans. It causes dissociation of ACTIN FILAMENTS.Gastric Emptying: The evacuation of food from the stomach into the duodenum.Adenylate Cyclase Toxin: One of the virulence factors produced by virulent BORDETELLA organisms. It is a bifunctional protein with both ADENYLYL CYCLASES and hemolysin components.Sweating: The process of exocrine secretion of the SWEAT GLANDS, including the aqueous sweat from the ECCRINE GLANDS and the complex viscous fluids of the APOCRINE GLANDS.Spider Venoms: Venoms of arthropods of the order Araneida of the ARACHNIDA. The venoms usually contain several protein fractions, including ENZYMES, hemolytic, neurolytic, and other TOXINS, BIOLOGICAL.Food Contamination: The presence in food of harmful, unpalatable, or otherwise objectionable foreign substances, e.g. chemicals, microorganisms or diluents, before, during, or after processing or storage.Entropion: The turning inward (inversion) of the edge of the eyelid, with the tarsal cartilage turned inward toward the eyeball. (Dorland, 27th ed)Acetylcholine: A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.Anal Canal: The terminal segment of the LARGE INTESTINE, beginning from the ampulla of the RECTUM and ending at the anus.Synaptosomes: Pinched-off nerve endings and their contents of vesicles and cytoplasm together with the attached subsynaptic area of the membrane of the post-synaptic cell. They are largely artificial structures produced by fractionation after selective centrifugation of nervous tissue homogenates.Complex Regional Pain Syndromes: Conditions characterized by pain involving an extremity or other body region, HYPERESTHESIA, and localized autonomic dysfunction following injury to soft tissue or nerve. The pain is usually associated with ERYTHEMA; SKIN TEMPERATURE changes, abnormal sudomotor activity (i.e., changes in sweating due to altered sympathetic innervation) or edema. The degree of pain and other manifestations is out of proportion to that expected from the inciting event. Two subtypes of this condition have been described: type I; (REFLEX SYMPATHETIC DYSTROPHY) and type II; (CAUSALGIA). (From Pain 1995 Oct;63(1):127-33)Urethral Diseases: Pathological processes involving the URETHRA.Movement Disorders: Syndromes which feature DYSKINESIAS as a cardinal manifestation of the disease process. Included in this category are degenerative, hereditary, post-infectious, medication-induced, post-inflammatory, and post-traumatic conditions.SNARE Proteins: A superfamily of small proteins which are involved in the MEMBRANE FUSION events, intracellular protein trafficking and secretory processes. They share a homologous SNARE motif. The SNARE proteins are divided into subfamilies: QA-SNARES; QB-SNARES; QC-SNARES; and R-SNARES. The formation of a SNARE complex (composed of one each of the four different types SNARE domains (Qa, Qb, Qc, and R)) mediates MEMBRANE FUSION. Following membrane fusion SNARE complexes are dissociated by the NSFs (N-ETHYLMALEIMIDE-SENSITIVE FACTORS), in conjunction with SOLUBLE NSF ATTACHMENT PROTEIN, i.e., SNAPs (no relation to SNAP 25.)Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Speech, Esophageal: A method of speech used after laryngectomy, with sound produced by vibration of the column of air in the esophagus against the contracting cricopharyngeal sphincter. (Dorland, 27th ed)Synaptic Transmission: The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.Deglutition Disorders: Difficulty in SWALLOWING which may result from neuromuscular disorder or mechanical obstruction. Dysphagia is classified into two distinct types: oropharyngeal dysphagia due to malfunction of the PHARYNX and UPPER ESOPHAGEAL SPHINCTER; and esophageal dysphagia due to malfunction of the ESOPHAGUS.Spores: The reproductive elements of lower organisms, such as BACTERIA; FUNGI; and cryptogamic plants.Trismus: Spasmodic contraction of the masseter muscle resulting in forceful jaw closure. This may be seen with a variety of diseases, including TETANUS, as a complication of radiation therapy, trauma, or in association with neoplastic conditions.Hypohidrosis: Abnormally diminished or absent perspiration. Both generalized and segmented (reduced or absent sweating in circumscribed locations) forms of the disease are usually associated with other underlying conditions.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Muscle Cramp: A sustained and usually painful contraction of muscle fibers. This may occur as an isolated phenomenon or as a manifestation of an underlying disease process (e.g., UREMIA; HYPOTHYROIDISM; MOTOR NEURON DISEASE; etc.). (From Adams et al., Principles of Neurology, 6th ed, p1398)Actinobacillosis: A disease characterized by suppurative and granulomatous lesions in the respiratory tract, upper alimentary tract, skin, kidneys, joints, and other tissues. Actinobacillus lignieresii infects cattle and sheep while A. equuli infects horses and pigs.Muscle Weakness: A vague complaint of debility, fatigue, or exhaustion attributable to weakness of various muscles. The weakness can be characterized as subacute or chronic, often progressive, and is a manifestation of many muscle and neuromuscular diseases. (From Wyngaarden et al., Cecil Textbook of Medicine, 19th ed, p2251)Pyloric Antrum: The region between the sharp indentation at the lower third of the STOMACH (incisura angularis) and the junction of the PYLORUS with the DUODENUM. Pyloric antral glands contain mucus-secreting cells and gastrin-secreting endocrine cells (G CELLS).Trigeminal Nerve Diseases: Diseases of the trigeminal nerve or its nuclei, which are located in the pons and medulla. The nerve is composed of three divisions: ophthalmic, maxillary, and mandibular, which provide sensory innervation to structures of the face, sinuses, and portions of the cranial vault. The mandibular nerve also innervates muscles of mastication. Clinical features include loss of facial and intra-oral sensation and weakness of jaw closure. Common conditions affecting the nerve include brain stem ischemia, INFRATENTORIAL NEOPLASMS, and TRIGEMINAL NEURALGIA.Abducens Nerve: The 6th cranial nerve which originates in the ABDUCENS NUCLEUS of the PONS and sends motor fibers to the lateral rectus muscles of the EYE. Damage to the nerve or its nucleus disrupts horizontal eye movement control.

Role of Rho and Rho kinase in the activation of volume-regulated anion channels in bovine endothelial cells. (1/1400)

1. We have studied the modulation of volume-regulated anion channels (VRACs) by the small GTPase Rho and by one of its targets, Rho kinase, in calf pulmonary artery endothelial (CPAE) cells. 2. RT-PCR and immunoblot analysis showed that both RhoA and Rho kinase are expressed in CPAE cells. 3. ICl,swell, the chloride current through VRACs, was activated by challenging CPAE cells with a 25 % hypotonic extracellular solution (HTS) or by intracellular perfusion with a pipette solution containing 100 microM GTPgammaS. 4. Pretreatment of CPAE cells with the Clostridium C2IN-C3 fusion toxin, which inactivates Rho by ADP ribosylation, significantly impaired the activation of ICl,swell in response to the HTS. The current density at +100 mV was 49 +/- 13 pA pF-1 (n = 17) in pretreated cells compared with 172 +/- 17 pA pF-1 (n = 21) in control cells. 5. The volume-independent activation of ICl,swell by intracellular perfusion with GTPgammaS was also impaired in C2IN-C3-pretreated cells (31 +/- 7 pA pF-1, n = 11) compared with non-treated cells (132 +/- 21 pA pF-1, n = 15). 6. Activation of ICl,swell was pertussis toxin (PTX) insensitive. 7. Y-27632, a blocker of Rho kinase, inhibited ICl,swell and delayed its activation. 8. Inhibition of Rho and of Rho kinase by the above-described treatments did not affect the extent of cell swelling in response to HTS. 9. These experiments provide strong evidence that the Rho-Rho kinase pathway is involved in the VRAC activation cascade.  (+info)

Lymphocyte migration through brain endothelial cell monolayers involves signaling through endothelial ICAM-1 via a rho-dependent pathway. (2/1400)

Lymphocyte extravasation into the brain is mediated largely by the Ig superfamily molecule ICAM-1. Several lines of evidence indicate that at the tight vascular barriers of the central nervous system (CNS), endothelial cell (EC) ICAM-1 not only acts as a docking molecule for circulating lymphocytes, but is also involved in transducing signals to the EC. In this paper, we examine the signaling pathways in brain EC following Ab ligation of endothelial ICAM-1, which mimics adhesion of lymphocytes to CNS endothelia. ICAM-1 cross-linking results in a reorganization of the endothelial actin cytoskeleton to form stress fibers and activation of the small guanosine triphosphate (GTP)-binding protein Rho. ICAM-1-stimulated tyrosine phosphorylation of the actin-associated molecule cortactin and ICAM-1-mediated, Ag/IL-2-stimulated T lymphocyte migration through EC monolayers were inhibited following pretreatment of EC with cytochalasin D. Pretreatment of EC with C3 transferase, a specific inhibitor of Rho proteins, significantly inhibited the transmonolayer migration of T lymphocytes, endothelial Rho-GTP loading, and endothelial actin reorganization, without affecting either lymphocyte adhesion to EC or cortactin phosphorylation. These data show that brain vascular EC are actively involved in facilitating T lymphocyte migration through the tight blood-brain barrier of the CNS and that this process involves ICAM-1-stimulated rearrangement of the endothelial actin cytoskeleton and functional EC Rho proteins.  (+info)

SNAP-25a and -25b isoforms are both expressed in insulin-secreting cells and can function in insulin secretion. (3/1400)

The tSNARE (the target-membrane soluble NSF-attachment protein receptor, where NSF is N-ethylmaleimide-sensitive fusion protein) synaptosomal-associated protein of 25 kDa (SNAP-25) is expressed in pancreatic B-cells and its cleavage by botulinum neurotoxin E (BoNT/E) abolishes stimulated secretion of insulin. In the nervous system, two SNAP-25 isoforms (a and b) have been described that are produced by alternative splicing. Here it is shown, using reverse transcriptase PCR, that messages for both SNAP-25 isoforms are expressed in primary pancreatic B and non-B cells as well as in insulin-secreting cell lines. After transfection, both isoforms can be detected at the plasma membrane as well as in an intracellular perinuclear region in the insulin-secreting cell line, HIT. To test for the functional role of the two isoforms in insulin secretion, mutant forms of SNAP-25a and b resistant against cleavage by BoNT/E were generated. Such mutant SNAP-25, when expressed in HIT cells, is not inactivated by BoNT/E and its ability to restore insulin secretion can thus be investigated. To obtain the toxin-resistant mutant isoforms, the sequence around the BoNT/E cleavage site (R176QIDRIM182) was changed to P176QIKRIT182. This is the sequence of the equivalent region of human SNAP-23 (P187-T194), which has been shown to be resistant to BoNT/E. The mutant SNAP-25 was resistant to BoNT/E in vitro and in vivo and both mutant isoforms were able to reconstitute insulin secretion from toxin-treated HIT cells.  (+info)

Involvement of RhoA and its interaction with protein kinase C and Src in CCK-stimulated pancreatic acini. (4/1400)

We evaluated intracellular pathways responsible for the activation of the small GTP-binding protein Rho p21 in rat pancreatic acini. Intact acini were incubated with or without CCK and carbachol, and Triton X-100-soluble and crude microsomes were used for Western immunoblotting. When a RhoA-specific antibody was used, a single band at the location of 21 kDa was detected. CCK (10 pM-10 nM) and carbachol (0.1-100 microM) dose dependently increased the amount of immunodetectable RhoA with a peak increase occurring at 3 min. High-affinity CCK-A-receptor agonists JMV-180 and CCK-OPE (1-1,000 nM) did not increase the intensities of the RhoA band, suggesting that stimulation of RhoA is mediated by the low-affinity CCK-A receptor. Although an increase in RhoA did not require the presence of extracellular Ca2+, the intracellular Ca2+ chelator 1, 2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-AM abolished the appearance of the RhoA band in response to CCK and carbachol. The Gq protein inhibitor G protein antagonist-2A (10 microM) and the phospholipase C (PLC) inhibitor U-73122 (10 microM) markedly reduced RhoA bands in response to CCK. The protein kinase C (PKC) activator phorbol ester (10-1,000 nM) dose dependently increased the intensities of the RhoA band, which were inhibited by the PKC inhibitor K-252a (1 microM). The pp60(c-src) inhibitor herbimycin A (6 microM) inhibited the RhoA band in response to CCK, whereas the calmodulin inhibitor W-7 (100 microM) and the phosphoinositide 3-kinase inhibitor wortmannin (6 microM) had no effect. RhoA was immunoprecipitated with Src, suggesting association of RhoA with Src. Increases in mass of this complex were observed with CCK stimulation. In permeabilized acini, the Rho inhibitor Clostridium botulinum C3 exoenzyme dose dependently inhibited amylase secretion evoked by a Ca2+ concentration with an IC50 of C3 exoenzyme at 1 ng/ml. We concluded that the small GTP-binding protein RhoA p21 exists in pancreatic acini and appears to be involved in the mediation of pancreatic enzyme secretion evoked by CCK and carbachol. RhoA pathways are involved in the activation of PKC and Src cascades via Gq protein and PLC.  (+info)

Bacterial toxins and the Rho GTP-binding protein: what microbes teach us about cell regulation. (5/1400)

In the present review activities of two bacterial toxins, Clostridium botulinum exoenzyme C3 and Escherichia coli CNF1, both acting on the GTP-binding protein Rho are analyzed. Proteins belonging to the Rho family regulate the actin cytoskeleton and act as molecular switches in a number of signal transduction pathways. C3 and CNF1 have opposite effects on Rho thus representing useful tools for studies on cell division, cell differentiation and apoptosis.  (+info)

Rho-dependent and -independent tyrosine phosphorylation of focal adhesion kinase, paxillin and p130Cas mediated by Ret kinase. (6/1400)

Glial cell line-derived neurotrophic factor (GDNF) signals through a unique receptor system that includes Ret receptor tyrosine kinase and a glycosyl-phosphatidylinositol-linked cell surface protein. In the present study, we have identified several proteins in neuroblastoma cells that are phosphorylated on tyrosine in response to GDNF. The phosphorylated proteins include focal adhesion kinase (FAK), paxillin and Crk-associated substrate, p130Cas, all of which are known to be associated with focal adhesions. Of these, paxillin and p130Cas interacted with Crk proteins in GDNF-treated neuroblastoma cells. GDNF also induced reorganization of the actin cytoskelton. Tyrosine phosphorylation of FAK, paxillin and p130Cas was inhibited by cytochalasin D or two specific inhibitors of phosphatidylinositol-3' kinase (PI-3' kinase), wortmannin and LY294002, indicating that their tyrosine phosphorylation depends on the formation of actin stress fiber and activation of PI-3' kinase. In addition, phosphorylation of FAK but not of paxillin and p130Cas was markedly impaired by the Clostridium botulinum C3 exoenzyme that specifically ADP-ribosylates and inactivates Rho. These results suggested the presence of Rho-dependent and -independent signaling pathways downstream of PI-3' kinase that mediate tyrosine phosphorylation of FAK, paxillin and p130Cas through Ret kinase.  (+info)

Tetanus and botulinum neurotoxins: mechanism of action and therapeutic uses. (7/1400)

The clostridial neurotoxins responsible for tetanus and botulism are proteins consisting of three domains endowed with different functions: neurospecific binding, membrane translocation and proteolysis for specific components of the neuroexocytosis apparatus. Tetanus neurotoxin (TeNT) binds to the presynaptic membrane of the neuromuscular junction, is internalized and transported retroaxonally to the spinal cord. The spastic paralysis induced by the toxin is due to the blockade of neurotransmitter release from spinal inhibitory interneurons. In contrast, the seven serotypes of botulinum neurotoxins (BoNTs) act at the periphery by inducing a flaccid paralysis due to the inhibition of acetylcholine release at the neuromuscular junction. TeNT and BoNT serotypes B, D, F and G cleave specifically at single but different peptide bonds, of the vesicle associated membrane protein (VAMP) synaptobrevin, a membrane protein of small synaptic vesicles (SSVs). BoNT types A, C and E cleave SNAP-25 at different sites located within the carboxyl-terminus, while BoNT type C additionally cleaves syntaxin. The remarkable specificity of BoNTs is exploited in the treatment of human diseases characterized by a hyperfunction of cholinergic terminals.  (+info)

SNARE complex formation is triggered by Ca2+ and drives membrane fusion. (8/1400)

Neurotransmitter exocytosis, a process mediated by a core complex of syntaxin, SNAP-25, and VAMP (SNAREs), is inhibited by SNARE-cleaving neurotoxins. Botulinum neurotoxin E inhibition of norepinephrine release in permeabilized PC12 cells can be rescued by adding a 65 aa C-terminal fragment of SNAP-25 (S25-C). Mutations along the hydrophobic face of the S25-C helix result in SNARE complexes with different thermostabilities, and these mutants rescue exocytosis to different extents. Rescue depends on the continued presence of both S25-C and Ca2+ and correlates with complex formation. The data suggest that Ca2+ triggers S25-C binding to a low-affinity site, initiating trans-complex formation. Pairing of SNARE proteins on apposing membranes leads to bilayer fusion and results in a high-affinity cis-SNARE complex.  (+info)

Clostridium botulinum is a taxonomic designation for at least four diverse species that are defined by the expression of one (monovalent) or two (bivalent) of seven different C. botulinum neurotoxins (BoNTs, A-G). The four species have been classified as C. botulinum Groups I-IV. The presence of bont genes in strains representing the different Groups is probably the result of horizontal transfer of the toxin operons between the species. Chromosome and plasmid sequences of several C. botulinum strains representing A, B, E and F serotypes and a C. butyricum type E strain were compared to examine their genomic organization, or synteny, and the location of the botulinum toxin complex genes. These comparisons identified synteny among proteolytic (Group I) strains or nonproteolytic (Group II) strains but not between the two Groups. The bont complex genes within the strains examined were not randomly located but found within three regions of the chromosome or in two specific sites within plasmids. A
Botulinum neurotoxins (BoNTs) produced by Clostridium botulinum are the most poisonous substances known to humankind. It is essential to have a simple, quick, and sensitive method for the detection and quantification of botulinum toxin in various media, including complex biological matrices. Our laboratory has developed a mass spectrometry-based Endopep-MS assay that is able to rapidly detect and differentiate all types of BoNTs by extracting the toxin with specific antibodies and detecting the unique cleavage products of peptide substrates. Botulinum neurotoxin type E (BoNT/E) is a member of a family of seven distinctive BoNT serotypes (A-G) and is the causative agent of botulism in both humans and animals. To improve the sensitivity of the Endopep-MS assay, we report here the development of novel peptide substrates for the detection of BoNT/E activity through systematic and comprehensive approaches. Our data demonstrate that several optimal peptides could accomplish 500-fold improvement in ...
0038]Botulinum toxin type A can be obtained by establishing and growing cultures of Clostridium botulinum in a fermenter and then harvesting and purifying the fermented mixture in accordance with known procedures. All the botulinum toxin serotypes are initially synthesized as inactive single chain proteins which must be cleaved or nicked by proteases to become neuroactive. The bacterial strains that make botulinum toxin serotypes A and G possess endogenous proteases and serotypes A and G can therefore be recovered from bacterial cultures in predominantly their active form. In contrast, botulinum toxin serotypes C1, D and E are synthesized by nonproteolytic strains and are therefore typically unactivated when recovered from culture. Serotypes B and F are produced by both proteolytic and nonproteolytic strains and therefore can be recovered in either the active or inactive form. However, even the proteolytic strains that produce, for example, the botulinum toxin type B serotype, only cleave a ...
The objective of the project is the development of in vitro detection methods for the different toxins (A, B, C, D, E and F) of Clostridium botulinum by optimizing both a competitive immuno-PCR test (icqPCR) and a quantitative immuno-PCR (iqPCR) and by comparing one to another with regard to the obtained specificity and sensitivity of detection for each type of botulinum toxin as well as to compare them to the reference method for detection of botulinum toxins being the mice toxicity test ...
Author summary The seven established Botulinum Neurotoxins serotypes (BoNT/A to G) and the many BoNT subtypes, the causative agents of botulism, are the most poisonous substances known (lethal doses in the low ng/kg range). Due to their toxicological properties, BoNTs are Janus-faced toxins: potent pathogenic factors and potential bioterrorism agents as well as safe and efficacious therapeutics. BoNTs exert their neuroparalytic action by cleaving SNARE proteins, either SNAP-25 or synaptobrevin/VAMP, which mediate neurotransmitter release at the neuromuscular junction; BoNT/C is the only serotype shown to cleave SNAP-25 and syntaxin-1 in vitro. Our study shows for the first time that this parallel cleavage also occurs in vivo. By using mutated toxins reported to be syntaxin-selective, we found that SNAP-25 proteolysis at the neuromuscular junction is the key determinant of BoNT/C lethality as it completely blocks nerve-muscle transmission. Conversely, syntaxin-1 cleavage only attenuates nerve terminal
The botulinum neurotoxins (BoNTs) are category A biothreat agents which have been the focus of intensive efforts to develop vaccines and antibody-based prophylaxis and treatment. Such approaches must take into account the extensive BoNT sequence variability; the seven BoNT serotypes differ by up to 70% at the amino acid level. Here, we have analyzed 49 complete published sequences of BoNTs and show that all toxins also exhibit variability within serotypes ranging between 2.6 and 31.6%. To determine the impact of such sequence differences on immune recognition, we studied the binding and neutralization capacity of six BoNT serotype A (BoNT/A) monoclonal antibodies (MAbs) to BoNT/A1 and BoNT/A2, which differ by 10% at the amino acid level. While all six MAbs bound BoNT/A1 with high affinity, three of the six MAbs showed a marked reduction in binding affinity of 500- to more than 1,000-fold to BoNT/A2 toxin. Binding results predicted in vivo toxin neutralization; NlAbs or MAb combinations that ...
Hyperactive glandular conditions are treated using topically formulated botulinum toxin compositions. In the preferred embodiment of the invention, topical botulinum preparations are applied directly to the skin by a patient as needed to suppress his or her hyperhidrosis, bromhidrosis, chromhidrosis, nevus sudoriferous, acne, seborrhiec dermatitis or other glandular condition. In other embodiments, topical botulinum toxins are applied with the aid of mechanical, electrical, and/or chemical transdermal delivery enhancers.
Background: Two decades ago, botulinum neurotoxin (BoNT) type A was introduced to the commercial market. Subsequently, the toxin was approved by the FDA to address several neurological syndromes, involving muscle, nerve, and gland hyperactivity. These syndromes have typically been associated with abnormalities in cholinergic transmission. Despite the multiplicity of botulinal serotypes (designated as types A through G), therapeutic preparations are currently only available for BoNT types A and B. However, other BoNT serotypes are under study for possible clinical use and new clinical indications; Objective: To review the current research on botulinum neurotoxin serotypes A-G, and to analyze potential applications within basic science and clinical settings; Conclusions: The increasing understanding of botulinal neurotoxin pathophysiology, including the neurotoxins effects on specific neuronal populations, will help us in tailoring treatments for specific diagnoses, symptoms and patients. Scientists and
Background: Two decades ago, botulinum neurotoxin (BoNT) type A was introduced to the commercial market. Subsequently, the toxin was approved by the FDA to address several neurological syndromes, involving muscle, nerve, and gland hyperactivity. These syndromes have typically been associated with abnormalities in cholinergic transmission. Despite the multiplicity of botulinal serotypes (designated as types A through G), therapeutic preparations are currently only available for BoNT types A and B. However, other BoNT serotypes are under study for possible clinical use and new clinical indications; Objective: To review the current research on botulinum neurotoxin serotypes A-G, and to analyze potential applications within basic science and clinical settings; Conclusions: The increasing understanding of botulinal neurotoxin pathophysiology, including the neurotoxins effects on specific neuronal populations, will help us in tailoring treatments for specific diagnoses, symptoms and patients. Scientists and
Clostridium botulinum Toxin A antibody [B364M] for ELISA, ICC/IF, RIA. Anti-Clostridium botulinum Toxin A mAb (GTX44113) is tested in Clostridium botulinum samples. 100% Ab-Assurance.
Myofascial pains are frequently found during the clinical examination of the patients presenting a painful chronic syndrome of the pelvis or the perineum. If the physiopathology of this component of the pain characterized by triggerpoints found in the clinical examination, remains uncertain; its coverage contributes to the improvement of the global pain of the patient. The physiotherapy can be useful but when it is not useful, we proposed injections of triggerpoints by local anesthetics. The injections of botulinum toxin on these triggerpoints have a legitimacy (action on the muscular cramp and action on the afferent fibers) but are they superior to the injections of local anesthetics of triggerpoints? The literature remains poor on the subject, justifying this randomized double-blind protocol comparing the efficacy of the botulinum toxin associated with a local anesthetic versus local anesthetic alone with a main criterion of evaluation in 2 months and a monthly follow-up as long as the patient ...
The botulinum toxin as a therapeutic agent: molecular and pharmacological insights Roshan Kukreja,1 Bal Ram Singh2 1Department of Chemistry and Biochemistry, University of Massachusetts, 2Botulinum Research Center, Institute of Advanced Sciences, Dartmouth, MA, USA Abstract: Botulinum neurotoxins (BoNTs), the most potent toxins known to mankind, are metalloproteases that act on nerve–muscle junctions to block exocytosis through a very specific and exclusive endopeptidase activity against soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins of presynaptic vesicle fusion machinery. This very ability of the toxins to produce flaccid muscle paralysis through chemical denervation has been put to good use, and these potentially lethal toxins have been licensed to treat an ever expanding list of medical disorders and more popularly in the field of esthetic medicine. In most cases, therapeutic BoNT preparations are high-molecular-weight protein complexes consisting of
Botulinum toxin (BTX) is a neurotoxic protein produced bi the bacterium Clostridium botulinum an relatit species.[1] It prevents the release o the neurotransmitter acetylcholine frae axon endins at the neuromuscular junction an thus causes flaccid paralysis. Infection wi the bacterium causes the disease botulism. The toxin is an aa uised commercially in medicine, cosmetics, an resairch. ...
Learn more about Botulinum Toxin Injections -- Medical at Regional Medical Center of San Jose DefinitionReasons for ProcedurePossible ComplicationsWhat to ExpectCall...
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Botulinum neurotoxin A (BoNT/A), mainly represented by subtype A1, is the most toxic substance known. It causes naturally-occurring food poisoning, and is among the biological agents at the highest risk of being weaponized. Several antibodies neutralizing BoNT/A by targeting its heavy chain (BoNT/A-H) have been isolated in the past. For the first time however, an IgG (4LCA) recently isolated by hybridoma technology and targeting the BoNT/A light chain (BoNT/A-L), was shown to inhibit BoNT/A endopeptidase activity and protect in vivo against BoNT/A. In the present study, a phage-displayed library was constructed from a macaque (Macaca fascicularis) hyper-immunized with BoNTA/L in order to isolate scFvs inhibiting BoNT/A endopeptidase activity for clinical use. Diversity of the scFvs constituting the library was limited due to the frequent presence, within the genes intended to be part of the library, of restriction sites utilized for its construction. After screening with several rounds of increasing
The clostridial neurotoxins (CNTs) comprise a family of eight related toxins: tetanus (TeNT) and seven botulinum neurotoxins (BoNT/A-G), which cause the disease...
Botulinum neurotoxins (BoNTs) are extremely potent toxins that are capable of causing death or respiratory failure leading to long-term intensive care. Treatment includes serotype-specific antitoxins, which must be administered early in the course of the intoxication. Rapidly determining human exposure to BoNT is an important public health goal. In previous work, our laboratory focused on developing Endopep-MS, a mass spectrometry-based endopeptidase method for detecting and differentiating BoNT/A-G serotypes in buffer and BoNT/A, /B, /E, and /F in clinical samples. We have previously reported the effectiveness of antibody-capture to purify and concentrate BoNTs from complex matrices, such as clinical samples. Because some antibodies inhibit or neutralize the activity of BoNT, the choice of antibody with which to extract the toxin is critical. In this work, we evaluated a panel of 16 anti-BoNT/A monoclonal antibodies (mAbs) for their ability to inhibit the in vitro activity of BoNT/A1, /A2, and ...
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We herein demonstrated that Tat PTD-mediated protein transduction was successfully applied to intact arterial strips. It was reported earlier that Clostridium botulinum exoenzyme C3 tagged with Tat PTD inhibited the urotensin-induced contraction in the rat aorta.29 In the present study, the introduction of the protein into the cells by Tat PTD was clearly proved by the observation of GFP fluorescence in the TAT-GFP-treated strips, and by immunoblot detection of Tat PTD-tagged MYPT1 fragments in the extract of the strips. The introduction of protein is also supported by the observation that the MYPT1 fragments enhanced the Ca2+-induced contraction only when tagged with Tat PTD. The time needed to obtain a significant enhancement of contraction suggested that the transduction of functional protein into the intact arterial strips takes place within 10 minutes, which is consistent with previous reports.22,23⇓. Treatment with TAT-MYPT11-374 enhanced the Ca2+-induced contraction with no effect on ...
This year, <"http://www.yourlawyer.com/topics/overview/botox">Botox was linked to a number of hospitalizations and 16 deaths. Of the deaths, four victims of the poisonous Botox injections were children. An additional 87 people were hospitalized. Botox and Myobloc have been linked to the injuries and fatalities because the botulinum toxin spread inside the bodies of the patients, killing some and injuring others. The toxin spreading in the bodies of the children proved most serious, killing four children under the age of 16. In addition to the deaths, there have been reported problems of muscle weakness and difficulty swallowing. American consumer group Public Citizen says it has seen 180 reports sent to the US Food and Drug Administration (FDA) about Botox and Myobloc.. Botulinum toxin, which is produced by the bacterium Clostridium botulinum and is known commercially as Botox and Myobloc, is one of the most powerful nerve poisons known. Although best known for smoothing facial ...
DESCRIPTION (provided by applicant): Botulinum neurotoxins (BoNT) are the most toxic substances known to humans causing respiratory failure upon poisoning. BoNTs lethality and ease of production has led to a category A bioterrorism agent designation for BoNT by the Department of Defense (DoD). Developing effective, post-exposure antagonists to BoNT is a top priority of the DoD. Despite their lethality, BoNTs have cosmetic and pharmaceutical applications and are currently FDA-approved for the treatment of glabellar lines (wrinkles), cervical dystonia, blepharospasm, cranial nerve VII disorders, and cosmoses. BoNT provides relief of muscle tension by silencing neurons that cause muscle contraction. For many disorders, BoNT-based treatments provide significant and long lasting reductions in pain. BoNTs exquisite specificity for neurons and long time of action make it a lead candidate for the treatment of neurological and muscle disorders where conventional treatments have failed. Development of ...
Botox is an injectable substance which is a medical grade form of the botulinum toxin, most often used to soften and relax forehead. Botulin toxin is compound produced by the bacterium Clostridium botulinum. It is an enzyme that helps in breaking down one of the fusion proteins that allow neurons to release acetylcholine at a neuromuscular junction. By interfering with nerve impulses in this way, it causes paralysis of muscles in botulism. Its been found that botox injections can help children with cerebral palsy from agravating and suffering some other side effects ...
sufferers, they are ineffective in stopping the painful side effects of teeth grinding, and do nothing for daytime tooth grinding.. Dentists have been injecting small doses of Botox directly into the large muscle that moves the jaw (masseter muscle) thereby successfully weakening it enough to stop involuntary grinding of the teeth and clenching of the jaw. Botox significantly relaxes the muscle, reducing the wear and tear on the teeth, due to grinding. Although it is not a cure for bruxism, Botox appears to effectively control uncomfortable symptoms better than a night guard for some patients, and treatment typically lasts for three to four months.. A downside emerged a number of years ago, though, showing evidence that Botox treatment may trigger a dramatic loss of bone density in the jaw. In a 2012 study in the journal Bone, "Rabbits were injected with botulinum toxin on one side of the jaw and researchers found that after four weeks, the bone in the injected side was severely decreased. ...
Botulinum NeuroToxin (BoNT) causes a potentially fatal disease called botulism. With an estimated LD50 of 1 ng/kg body weight, the family of BoNT serotypes, subdivided into more than 40 subtypes, are the most toxic naturally occurring substances known. The most widely accepted method for BoNT detection is the Mouse Lethality Bioassay (MLB) which has a sensitivity of 10-100 pg/mL. However, respiratory failure is the end point, large numbers of mice are required for serotyping and quantitation (, 100 per sample), and it has variable sensitivity and long readout times of 1-4 days. The purpose of the Botulinum NeuroToxin BLD-Test Performance Study is to validate a recently developed molecular-based BoNT assay so that it may be successfully adapted to replace the MLB for detecting and distinguishing the disease causing serotypes in a range of matrices (e.g. food, beverage, environmental, and human and animal samples collected for diagnostic purposes). The BLD-Test employs an automated, portable ...
The Australasian College of Cosmetic Surgery estimated that 1.5 million botulinum toxin injections or 250,000 wrinkle reduction procedures were administered in Australia in 2009. These figures are 30% higher than those reported for 2008. With the need for further and ongoing treatment in those who have previously received injections and the promise of new customers, these numbers are expected to double over the next five years. There are two formulations of botulinum toxin available for injection in Australia: • BOTOX® • DYSPORT® Both are purified from the toxic bacterium, Clostridium botulinum. This bacterium has a claim to fame as the cause of the rare but serious condition known as botulism. In this condition, ingestion of food or water contaminated with the bacterium or the toxins it produces, leads to progressive paralysis.. This usually starts with the muscles of the face and eyes and then spreads progressively over the body. It affects the face and eyes first because these are among ...
In managing patients with spasticity, especially when injecting botulinum toxin, there is one motto that holds true. Its that the more one thinks he knows the more there really is to learn. Whether it is patient criteria, medication use or muscle selection for injection, nothing is as straight forward as it seems.. It is the goal of this article to review the factors that form the basis for selection of botulinum toxin therapy in adult patients. The features of botulinum type A and type B will be compared. Finally, techniques and resources available to the clinician in determining when botulinum might be effective and in which muscles will be introduced.. When considering spasticity management the physician needs to take into account the patients physical presentation as well as the goals that they and their care providers have. Positive symptoms of upper motor syndrome include spasticity, heightened reflexes, clonus, and synergy patterns of movement.. Negative symptoms include weakness and ...
Apparatus, systems and methods can provide improved detection of botulinum neurotoxins. In one aspect an isoquinolynyl compound can be used to enhance the sensitivity of both Forster resonance energy
Find Botulinum and Tetanus Neurotoxins (BoNT and TeNT) research area related information and Botulinum and Tetanus Neurotoxins (BoNT and TeNT) research products from R&D Systems. Learn more.
Clostridium botulinum produces a transcription factor that can aggregate and self-propagate a prion-like form, leading to genome-wide changes in gene expression in E. coli, according to a study.. 1 Comment. ...
Clostridium botulinum produces a transcription factor that can aggregate and self-propagate a prion-like form, leading to genome-wide changes in gene expression in E. coli, according to a study.. 1 Comment. ...
The Botulinum Journal from Inderscience Publishers provides an international forum and refereed authoritative source of information encompassing varied fields involved with botulinum neurotoxins
Botox is a wrinkle treatment derived from the bacteria Clostridium botulinum. Learn how this versatile agent came to be as well as its other uses.
Botulinum: We have been blocking the deeply embedded and hardwired consequences of tens of millions of years of evolutionary trial-and-error product testing, writes Will Cairns
Syn®-ake designed to work much like Botox, which reduces muscular contractions in the face and reduces cell movement; thereby keeping the skin smooth. Syn-ake is a synthesized peptide that mimics the effects of the toxin produced by the bacteria Clostridium Botulinum Swiss Apple Stem Cell protects the longevity of the skins stem cells, helping to combat the aging process while improving skin renewal Peptides complex amino acids with multi-functional capacity to signal enzymes, promote collagen and relax muscle fibers and iron out the wrinkle. Vitamin C eases and prevents redness and dark circles while energizing the skin. Resveratrol assists the anti-aging process by delivering antioxidants and acting as a skin protectant, effectively preventing premature aging of skin cells. Hyaluronic Acid allows the skin to increase moisture retention, helping to improve skin elasticity as we age. Neodermyl® increases synthesis of collagen I & III (youth collagen) and elastin, helping to improve skin ...
This study is comparing the efficacy of botulinum toxin A [Dysport] injections in treatment-naive versus pre-treated patients (early-start vs medium-start vs
subtype A4 neurotoxin (BoNT/A4) is naturally expressed in the dual-toxin-producing strain 657Ba in 100 lower titers than BoNT/B. the clostridial appearance system. Comparative analyses of the actions of rBoNT/A4-L260F and rBoNT/A4 I264R demonstrated 1, 000-fold-lower activity than BoNT/A1 in both nonmutated and mutated BoNT/A4. This indicates these mutations usually do not alter the experience of BoNT/A4 holotoxin. In conclusion, a recombinant BoNT from a dual-toxin-producing stress was purified and portrayed within an endogenous clostridial appearance program, allowing analysis of the toxin. Launch Botulinum neurotoxins (BoNTs) will be the most poisonous chemicals known and so are produced by specific types. ...
2) Even small amounts of participation is appreciated: This works better for first year students who often have little clinical experience, but I think it does help even with more experienced learners. In the botulinum toxin injection clinic, I will have the students only observe for the first day or so. After that I have them clean the injection area with alcohol swabs, and hook up the EMG ground and reference leads. Although that doesnt sound like much, for a student, it makes them understand that they are being helpful and are a valued part of your team. In truth, it does make things go faster as it takes about the same amount of time to wash my hands as it does to prep the patient for the injections. As possible, I also try to let the students do one injection in a relatively straight forward site by the end of the ten weeks. It doesnt always work out that a good patient/ injection works out on the last day of the rotation. But, even doing one injection for a student is potentially a big ...
Recovery of neuronal function is critical for overcoming botulinum neurotoxin (BoNT)-mediated paralysis. Strategies for promoting such recovery have proven near...
The database will only include epitopes of less than 50 residues in either a linear or conformational sequence. If the epitope is non-peptidergic, the mass restriction is to be less than 5000 Daltons to be included in the database. Important Exception: Epitopes greater than 50 residues will be curated for certain pathogens including Botulinum toxin and anthrax epitopes. A region or fragment of ,50aa from B. anthracis and C. botulinum will be curated as an epitopic region in the following cases: ...
What kinds of information are actually stored in DNA? Several kinds, but bottom line, DNA is primarily a system for specifying sequences of amino acids. The information is stored as three-letter "words" (GCA, ATG, TCG, etc.) called codons. There are 64 possible length-3 words in a system that uses a 4-letter alphabet. Fortunately, there are only 20 amino acids. I say "fortunately," because imagine if there were 64 different amino acids (as there might be in extra-terrestrial life, say) and they had to occur in roughly equal amounts in all proteins. Every possible codon would have to be used (in roughly equal numbers) and there would be no possibility of an organism like C. botulinum developing a "preference" for A or T in its DNA. It is precisely because only 20 codons out of a possible 64 need be used that organisms like C. botulinum (with a huge imbalance of AT vs. GC in its DNA) can exist ...
What kinds of information are actually stored in DNA? Several kinds, but bottom line, DNA is primarily a system for specifying sequences of amino acids. The information is stored as three-letter "words" (GCA, ATG, TCG, etc.) called codons. There are 64 possible length-3 words in a system that uses a 4-letter alphabet. Fortunately, there are only 20 amino acids. I say "fortunately," because imagine if there were 64 different amino acids (as there might be in extra-terrestrial life, say) and they had to occur in roughly equal amounts in all proteins. Every possible codon would have to be used (in roughly equal numbers) and there would be no possibility of an organism like C. botulinum developing a "preference" for A or T in its DNA. It is precisely because only 20 codons out of a possible 64 need be used that organisms like C. botulinum (with a huge imbalance of AT vs. GC in its DNA) can exist ...
u.n. owen: I certainly believe you- the most important thing is to listen to your body. One of the above links states that something like 15% of the population is sensitive to MSG, and the symptomology ranges from nervous energy to the kind of experience that you had. I used to avoid MSG as a matter of course, basically because I didnt know what it was, exactly. I found out a while ago, and having no detectable problems, I am not averse to foods containing it. As Malor stated earlier in the thread, a LOT of foods that have natural flavoring in the ingredient list have MSG. If you folks want to talk about real neurotoxins, we shouldnt forget C. botulinum or tetrodotoxin, the carefully-removed component of fugu ...
The Bon-Ton Stores, Inc. (NASDAQ: BONT) today reported results for the third quarter of fiscal 2012 ended October 27, 2012....BONT
This entry lacks etymological information. If you are familiar with the origin of this term, please add it to the page per etymology instructions. You can also discuss it at the Etymology scriptorium ...
Botulinum Toxin Therapy for Chronic Migraine What is botulinum toxin? Botulinum toxin (Onabotulinum Toxin A) is made from a toxin produced by the bacterium Clostridium botulinum. In high doses it can produce muscle paralysis. In low doses, it is used to treat many conditions. Botulinum toxin is a medicine approved by the FDA to prevent chronic migraines. How does it work? It is unclear how botulinum toxin treats chronic migraine. Botulinum toxin injections can cause relaxation of muscles and can block nerve signal transmission. The effects last about 12 weeks. It works best if treatment is done every 12 weeks. It may take more than one treatment to feel the full effect of botulinum toxin therapy. How do I know it will help me? Botulinum toxin treatments are expensive and come with some risk. Both your provider and insurance consider this treatment when less invasive treatments have not worked for you. Botulinum toxin has been found to work well for chronic migraine. Most people (up to 70%) feel ...
Humeral lateral epicondylitis or tennis elbow is a common painful elbow disorder. The cause of tennis elbow is the chronic overload of bone-tendon junction. High prevalence of tennis elbow has a direct impact on the workplace productivity and quality of life. Steroid injection is the very few methods proved to have short-term efficacy in tennis elbow treatment, but it has potential adverse effects like tendon rupture. Temporary paralysis of muscle after botulinum toxin injection may reduce the physical demands and facilitate the normal repair mechanism during recovery. Preliminary studies suggested that botulinum toxin injection is effective in treating tennis elbow. The objective of this study is to compare the effects of botulinum toxin injection with corticosteroid injection in tennis elbow treatment ...
Gentaur molecular products has all kinds of products like :search , ListBio \ QD Botulinum Neurotoxin Type A Complex from Clostridium botulinum1,3,4 \ 9128B for more molecular products just contact us
Grass sickness is an often fatal disease affecting horses especially in the springtime and leading to different signs of neurotoxicity. The pathogenesis still remains unclear, but there seems be a toxicoinfection with the neurotoxin-producing bacterium clostridium botulinum and the disease.
Repeated botulinum toxin injection for idiopathic overactive bladder: will chemodenervation become a long-term solution?: Botulinum toxin A (BTX-A) has emerged
NIH Funding Opportunities and Notices in the NIH Guide for Grants and Contracts: Development of In-Vitro Assays to Assess the Potency of Botulinum Neurotoxin Type A (SBIR [R43/R44]) PA-09-179. NINDS
NIH Funding Opportunities and Notices in the NIH Guide for Grants and Contracts: Development of In-Vitro Assays to Assess the Potency of Botulinum Neurotoxin Type A (STTR [R41/R42]) PA-09-178. NINDS
Botulinum toxin is one of the most toxic natural substances; it acts by blocking the neuromuscular transmission by inhibiting Acetylcholine (Ach) releasing from the motor nerve into the neuromuscular junction. Although the toxin inhibits ACh release, other transmitters can also be inhibited. Botulinum toxin, specifically toxin type A (BONT-A) has been used since the 1970s to treat many different disorders, such as general spasticity resulting from stroke, multiple sclerosis or cerebral palsy, strabismus, hyperhidrosis or excessive sweating, pain, and it is effective in combating migraine and tension headaches. Since prostate gland is under the influence of autonomic innervation and associated neurotransmitters, the effects of BONT-A on the prostate have gained attention in the urological community and it has been studied in different species, including rats, dogs and humans. The aim of this paper is to review the mechanism of action of botulinum toxin and to discuss in particular the results of ...
Botulism is a serious illness that causes flaccid paralysis of muscles. It is caused by a neurotoxin, generically called botulinum toxin, that is produced by the bacterium Clostridium botulinum. There are seven distinct neurotoxins (types A-G) that Clostridium botulinum produce, but types A, B, and E (rarely F) are the most common that produce the flaccid paralysis in humans. The other types mainly cause disease in animals. Most Clostridium species produce only one type of neurotoxin.. ...
The carboxy-terminal domain of the heavy chain recognizes a specific binding site, while the nitrogen-terminus transports the lighter chain into the nerve cytosol (Peck et al. 2010). The lighter chain contains metalloproteases that target specific proteins involved in controlling the exocytosis machinery (Verderio et al. 2006). The inhibition of this integral machinery stops the release of acetylcholine and the neuron fails to send an important signal throughout the body. The lighter chain also decreases the stability of the binding complex, further preventing acetylcholine from being able to bind to the synaptic vesicles (Peck et al. 2010). In addition to releasing neurotoxins when exposed to varying environmental conditions, Clostridium botulinum also increases production of proteases that are secreted from the cell to breakdown polypeptides to contribute to contaminating food and therefore increasing its own toxicity. A large proportion of the bacterias genome encodes for several different ...
Kuo, in a study assessing whether suburothelial injection of different doses of botulinum toxin A would have a similar therapeutic effect to but less side effects than the use of 200 U botulinum toxin... more
Toxic proteins produced from the species CLOSTRIDIUM BOTULINUM. The toxins are synthesized as a single peptide chain which is processed into a mature protein consisting of a heavy chain and light chain joined via a disulfide bond. The botulinum toxin light chain is a zinc-dependent protease which is released from the heavy chain upon ENDOCYTOSIS into PRESYNAPTIC NERVE ENDINGS. Once inside the cell the botulinum toxin light chain cleaves specific SNARE proteins which are essential for secretion of ACETYLCHOLINE by SYNAPTIC VESICLES. This inhibition of acetylcholine release results in muscular PARALYSIS ...
Botulinum toxin injection bilateral rectus femoris, medial hamstrings, and gastrocnemius soleus muscles, phenol neurolysis of bilateral obturator nerves, application of bilateral short leg fiberglass casts.
Botulism is caused by a neurotoxin produced from the anaerobic, spore-forming bacterium Clostridium botulinum. Botulism in humans is usually caused by toxin types A, B, and E. Since 1973, a median of 24 cases of foodborne botulism, 3 cases of wound botulism, and 71 cases of infant botulism have been reported annually to the Centers for Disease Control and Prevention (CDC). New vehicles for transmission have emerged in recent decades, and wound botulism associated with black tar heroin has increased dramatically since 1994. Recently, the potential terrorist use of botulinum toxin has become an important concern.. Botulism is characterized by symmetric, descending, flaccid paralysis of motor and autonomic nerves, usually beginning with the cranial nerves.Blurred vision, dysphagia, and dysarthria are common initial complaints. The diagnosis of botulism is based on compatible clinical findings; history of exposure to suspect foods; and supportive ancillary testing to rule out other causes of ...
The overall goals of this project were to develop sensitive and specific micro-scale detection systems for botulinum neurotoxin (BoNT) that can be used to detect BoNT in intentionally adulterated foods or other samples and quickly communicate detection events using wireless technology. Additionally, the liquid crystal sensing component of the system lends itself to integration with food packaging to provide visual indicators of contamination. By developing and merging two sensing methods, (a) biomembrane sensing and bio-electronic transduction and (b) liquid crystal-based sensors, this project has involved into an integrated, wireless, modular platform for sensing botulinum toxin (BoNT). During this project, our laboratories successfully carried out a multidisciplinary collaboration to develop sensing platforms for botulinum neurotoxins (BoNTs) based on microfluidics and liquid sensor platforms. Wireless and optical sensing for biological toxins was also a method developed in this the project ...
In an abstract (Botulinum neurotoxin vaccines: past present, and future), published by PubMed back in 2007, Smith, LA and Rusnak JM detail that In the early 1930s, a formalin-inactivated toxoid against botulium neurotoxin was first tested in humans. In 1965, a pentavalent botulinum toxiod (PBT) received Investigational New Drug (IND) status under the Centers for Disease Controls IND 161 (for at risk workers), and in 1991 under the United States Armys Office of the Surgeon General IND 3723 (for military deployment). This PBT vaccine has been shown to be safe with over 20,000 injections given to date, and continues to be used in at risk individuals. During the past decade, recombinant DNA technology has been employed to develop second generation vaccines to prevent botulism. Recombinant subunit vaccines utilizing the receptor-binding domains of botulinum neurtoxin (BoNT) have been shown to be safe and efficacious in protecting animal models against BoNT serotypes A, B, C1, D, E and F. In 2004, ...
Shop Ras-related C3 botulinum toxin substrate ELISA Kit, Recombinant Protein and Ras-related C3 botulinum toxin substrate Antibody at MyBioSource. Custom ELISA Kit, Recombinant Protein and Antibody are available.
The basics of Botulinum Toxin (BT) are important to understand when considering injections. Botulinum toxin (BT) is a safe neuromodulator agent.
TY - JOUR. T1 - Botulinum toxin A for lower facial contouring. T2 - A prospective study. AU - Yu, Chung Chih. AU - Chen, Philip Kuo Ting. AU - Chen, Yu Ray. PY - 2007/10/1. Y1 - 2007/10/1. N2 - Background: A prominent mandibular angle is a common reason for aesthetic treatment among Asian women. Such women usually present with hypertrophic masseteric muscles, and one treatment for this uses botulinum toxin A (BoNTA). Detailed effectiveness and physiologic influences of this therapy are still under investigation. Methods: The authors report a prospective study of 10 female volunteers with hypertrophic masseteric muscles who received a single treatment comprising intramuscular injection of BoNTA. The facial change and the discomfort of the injection were self-rated using a visual analog scale, and the patients were regularly inspected up to 1 year. Bite forces also were measured for chronological documentation. Volume changes of masticating muscles were evaluated by three-dimensional computed ...
The Toxin . . . . . . . Tips and Tricks . . . . . . References . . . . . . . 21 21 22 22 22 22 22 22 22 22 22 23 24 24 The requirements and rules are basically the same for every aesthetic procedure. The following list is not intended to give a complete overview but to give some hopefully helpful advice when treating aesthetic indications with botulinum toxin (BNT). 2 Documentation A thorough documentation of all treatment-related data is highly recommended. Besides being useful for legal and billing reasons, thorough documentation will help to improve ones own performance and thus patients satisfaction, too. Botulinum toxin is a powerful agent for the upper third: it can erase wrinkles, lift the eyebrows and improve the eye contour. If the patient presents severe photo-damage, the skin of the three thirds is compromised and what can be improved in the skin appearance in the upper third, can barely be achieved in the lower and even less in the mid third. The question that should be asked now ...
BACKGROUND AND PURPOSE: Conventional scales measure the effect of botulinum toxin (BT) therapy only at specific points in time. The Dystonia Discomfort Scale (DDS), a novel, easy-to-use, self-assessment scale to record temporal profiles of the effect of BT therapy in cervical dystonia (CD), is introduced and evaluated against the Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS).
Looking for online definition of C. botulinum in the Medical Dictionary? C. botulinum explanation free. What is C. botulinum? Meaning of C. botulinum medical term. What does C. botulinum mean?
Adverse effects of botulinum neurotoxin A in spasticity management. Joshi, Tapan N.; Joshi, Sonal // International Journal of Nutrition, Pharmacology, Neurological D;Jul2011, Vol. 1 Issue 2, p126 The article focuses on the review of the probable adverse effects of botulinum neurotoxin A and the pathogenesis for managing spasticity. It states that botulinum neurotoxin is used to block the spread of active nerve impulses and to avoid serious side effects such as muscle weakness and... ...
Food borne botulism is a severe intoxication caused by eating the preformed toxin present in contaminated food.. Food borne botulism occurs when the bacterium Clostridium botulinum is allowed to grow and produce toxin in food that is later eaten without sufficient heating or cooking to inactivate the toxin. Botulinum toxin is one of the most potent neurotoxins known.. Typically in a few hours to several days after you eat the contaminated food you will start to show the classic symptoms; blurred vision, dry mouth, and difficulty in swallowing. Gastrointestinal symptoms may or may not occur. If untreated, the paralysis always descends through the body starting at the shoulders and working its way down.. Celebrate Christmas and New Years Eve in Rome!. The most serious complication of botulism is respiratory failure where it is fatal in up to 10% of people. It may take months before recovery is complete.. If the disease is caught early enough it can be treated with antitoxin. If paralysis and ...
Botulinum toxin type A (BoNT-A) (Botox®, Myobloc™, Dysport®, Xeomin™) is a naturally occurring toxin produced by the Clostridium botulinum bacterium.
Food contaminated with Clostridium botulinum toxin may not look or smell spoiled but can still make you sick. Symptoms can include nausea, vomiting, fatigue, dizziness, blurred or double vision, dry mouth, respiratory failure and paralysis. In severe cases of illness, people may die. ...
Mouse monoclonal antibody raised against Clostridium botulinum D Toxoid. Clostridium botulinum D toxoid (MAB0406) - Products - Abnova
The Fairfield Medical Center reported on Tuesday seeing a number of patients exhibiting symptoms of the a rare, paralytic, foodborne illness botulism in people who were attending a potluck on Sunday, April 19 at the Cross Pointe Free Will Baptist Church in Lancaster. Approximately 60 people attended the event.. Botulism is not infectious, and cannot be spread from person-to-person.. Botulism anti-toxin is being supplied by the Centers for Disease Control and Prevention (CDC) to treat the patients, according to the Fairfield County Health Department. As of Tuesday the patients were on ventilators awaiting the anti-toxin. At least five were considered to be in critical condition.. Food borne botulism is a severe intoxication caused by eating the preformed toxin present in contaminated food.. Food borne botulism occurs when the bacterium Clostridium botulinum is allowed to grow and produce toxin in food that is later eaten without sufficient heating or cooking to inactivate the toxin. Botulinum ...
Objective: To determine the safety and the self-reported efficacy of botulinum toxin injections for adult spasticity in current clinical practice. Design: A prospective observational study. Subjects: A total of 406 adult patients with focal spasticit
First lets get an overview of what botulism is. Botulism is an illness that causes varying degrees of paralysis in the body from a toxin produced by the bacteria Clostridium botulinum. C. botulinum is practically everywhere - just about anything thats touched soil will contain spores. So why dont we get sick from it all the time? Most of the time this bacteria is dormant, and its only when conditions are right that it grows and makes this toxin. C. botulinum prefers an anaerobic (oxygen-free) environment thats not too acidic, not too salty, not too crowded with other bacteria, and it does especially well at warm temperatures. A unique characteristic of C. botulinum is its ability to survive high temperatures for relatively long periods of time ...
Botulism Definition Botulism is an acute, progressive condition caused by botulinum toxin, a natural poison produced by the spore-forming bacteria Clostridium botulinum.
Read about outbreaks of botulism poisoning, causes (Clostridium botulinum toxin), symptoms (muscle paralysis, dry mouth, constipation), history, treatment, and types (foodborne, infant, wound). The botulinum toxin is one of the most lethal known substances.
Catalyzes the attachment of glutamate to tRNA(Glu) in a two-step reaction: glutamate is first activated by ATP to form Glu-AMP and then transferred to the acceptor end of tRNA(Glu).
General Information: Clostridium botulinum Ba4 str. 657 was isolated from an infant botulism case in 1976. The strain is a bivalent Ba strain, that simultaneously produces two different toxin types. This organism produces one of the most potent and deadly neurotoxins known, a botulinum toxin that prevents the release of acetylcholine at the neuromuscular junction, thereby inhibiting muscle contraction and causing paralysis. In most cases the diseased person dies of asphyxiation as a result of paralysis of chest muscles involved in breathing. The spores are heat-resistant and can survive in inadequately heated, prepared, or processed foods. Spores germinate under favorable conditions (anaerobiosis and substrate-rich environment) and bacteria start propagating very rapidly, producing the toxin.Botulinum toxin, and C. botulinum cells, has been found in a wide variety of foods, including canned ones. Almost any food that has a high pH (above 4.6) can support growth of the bacterium. Honey is the ...
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class="publication">Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href="http://www.nrbook.com/b/bookcpdf.php">Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
Background Botulinum neurotoxin (BoNT) may be the strongest poison recognized to mankind. a style like the separation from the BoNT-A light string through the holotoxin. This medication delivery vehicle could possibly be used to provide BoNT-A antidotes into BoNT-A intoxicated cultured mouse spinal-cord cells. Conclusion A highly effective BoNT-based medication delivery vehicle may be used to straight deliver toxin inhibitors into intoxicated nerve terminal cytosol. This process could possibly be used for targeted medication delivery to buy 315183-21-2 take care of additional neuronal and neuromuscular disorders. This record also provides fresh understanding of endocytosis and exocytosis aswell by BoNT trafficking. History Botulinum neurotoxins (BoNTs) are made by the anaerobic em Clostridium botulinum /em varieties of bacteria and so are the reason for botulism, a life-threatening neuroparalytic disease. They are really potent meals poisons, having a mouse LD50 of 0.1 ng/kg for type A [1,2]. ...
Producer of Botulinum Toxin type A, offers information on treatment and answers to common questions, a searchable list of physicians, surveys, testimonials, and beauty tips. ...
...LA JOLLA Calif. February 23 2012 Researchers at Sanford-Burnham Me... Now that we better understand the structure of the bacterial machiner... The Janus-faced toxin ...The botulinum neurotoxin is two-faced. On one side its the most pois...,Disarming,the,botulinum,neurotoxin,biological,advanced biology technology,biology laboratory technology,biology device technology,latest biology technology
Get this from a library! Botulinum toxin A for spasticity and associated pain following damage to the central nervous system : clinical and cost effectiveness and guidelines for use. [Sarah Ndegwa; Carolyn Spry; Canadian Agency for Drugs and Technologies in Health. Health Technology Inquiry Service.]
Chemical Alley How easy was it to buy an eye-popping 3,081 vials of research botulinum toxin, the deadly neurotoxin produced by Clostridium botulinum, always found on jihadist terror wish lists? Very easy in 2003 - unlike so many other things alleged to be simple to do by designated evil-doers in the war on terror. Two Arizona scammers in pursuit of profit in the anti-aging industry found it elementary to order the most poisonous substance known fresh from List Labs in Campbell, CA, a purifier of biochemicals and toxins used in counter-terror research.. Chad Livdahl and Zahra Karim had set up a series of shell companies in Tucson with the aim of acquiring botulinum toxin cheaply and repackaging it as "Mimic Botox." The "Mimic Botox" would be shilled to cosmetic surgeons, fraudulently misrepresented as Botox, undercutting Allergans product, the only company that can sell it as a trademarked and licensed drug.. The scam worked. Using the front company Toxins Research International, Livdahl and ...
The purpose of this clinical investigation is to confirm the efficacy of eliminating facial wrinkles by injecting botulinum toxin A into mimetic muscles. Fifty-four patients were injected with BOTOX A-14 in the corrugator superciliaris, 19 in the fro
Find out more information about the myths and fact about Botulinum Toxin (Botox) and its uses. Visit Harley Street MD website today!
Botulinum toxin may help prevent shaking or tremor in the arms and hands of people with multiple sclerosis (MS), according to new research published in the July 3, 2012, print issue of Neurology.
Dr Nikola Milojevic explains how dermal fillers, botulinum toxin and plasma can be used to address the signs of ageing in the upper and lower eye. ...
Scientists have discovered the first new form of botulinum toxin in over 40 years, but theyre taking the unusual step of keeping key details about it
Scientists have discovered the first new form of botulinum toxin in over 40 years, but they're taking the unusual step of keeping key details about it
BioAssay record AID 329446 submitted by ChEMBL: Inhibition of Clostridium botulinum recombinant BoNT/A light chain toxin expressed in Escherichia coli by FRET assay.
Botulism is a rare but very serious type of food poisoning caused by toxins produced by bacteria ( Clostridium botulinum ) that are commonly found in soil. Botulism is often caused by food that is not home-canned properly, such as home-canned beans and corn. In children younger than 1 year, botulism may be caused by...
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Botulism Symptoms and Treatments in Dogs - Botulism is a paralytic disease caused by neurotoxins produced by the bacteria Clostridium botulinum.
C.L.I.M.B.®, an injection training program for Dysport® (abobotulinumtoxinA). Read Important Safety Information & Boxed Warning.
Reaktivität: Bakterien Wirt: Maus Klon: KBA468 Konjugat: DyLight 350 | Clostridium Botulinum A Toxoid Antikörper (ABIN4263832).
Reaktivität: Bakterien Wirt: Maus Klon: KBA468 Konjugat: Alexa Fluor 405 | Clostridium Botulinum A Toxoid Antikörper (ABIN4263840).
... is used to treat a number of problems. Muscle spasticity[edit]. Botulinum toxin is used to treat a number of ... Botulinum toxin produced by Clostridium botulinum is the cause of botulism.[9] Humans most commonly ingest the toxin from ... Botulinum toxin A is marketed under the brand names Botox and Xeomin. Botulinum toxin B is marketed under the brand name ... when samples containing botulinum toxin are tested.[citation needed] To confirm a diagnosis of botulinum toxin poisoning, ...
Botulinum toxin type A[edit]. Local intradermal injection of botulinum neurotoxin type A may be helpful in chronic focal ... Mittal, SO; Safarpour, D; Jabbari, B (February 2016). "Botulinum Toxin Treatment of Neuropathic Pain". Seminars in Neurology. ... toxins, remote manifestations of malignancies, immune mediated disorders and physical trauma to a nerve trunk.[7][8] ...
Botulinum toxin. Centrally acting. Carbamic acid esters. *Carisoprodol. *Cyclarbamate. *Difebarbamate. *Febarbamate. * ...
Botulinum toxin. *v. *t. *e. *Agents used in chemical warfare. *incapacitation. *riot control ...
Botulinum toxin. Centrally acting. Carbamic acid esters. *Carisoprodol. *Cyclarbamate. *Difebarbamate. *Febarbamate. * ...
SNAP-25 inactivators: Botulinum toxin (A, C, E). *VAMP inactivators: Botulinum toxin (B, D, F, G) ...
Botulinum toxin. Centrally acting. Carbamic acid esters. *Carisoprodol. *Cyclarbamate. *Difebarbamate. *Febarbamate. * ...
Botulinum toxin. Centrally acting. Carbamic acid esters. *Carisoprodol. *Cyclarbamate. *Difebarbamate. *Febarbamate. * ...
Biological Toxins[edit]. Main article: Toxin. *X - botulinum toxin A. *XR - partially purified botulinum toxin A ...
Muscarinic toxin 7. *N-Ethyl-3-piperidyl benzilate. *N-Methyl-3-piperidyl benzilate ...
SNAP-25 inactivators: Botulinum toxin (A, C, E). *VAMP inactivators: Botulinum toxin (B, D, F, G) ...
Botulinum toxin (BTX). *Tetanospasmin (TeNT). *Chlorophenylsilatrane. *Tetrodotoxin. Nettle. *Phosgene oxime (CX). Pulmonary/ ...
The surgery is for those who do not respond to physical therapy or botulinum toxin injection or have a very fibrotic ... Safarpour, Yasaman; Jabbari, Bahman (2018-02-24). "Botulinum Toxin Treatment of Movement Disorders". Current Treatment Options ... Samotus, Olivia; Lee, Jack; Jog, Mandar (2018-03-20). "Personalized botulinum toxin type A therapy for cervical dystonia based ...
"Botulinum toxin injections". www.aesthetika.co.uk. Retrieved 30 August 2015. Video at University of Utah. ... ISBN 978-0-7817-9121-2. Kipioti A, Taylor R (2003). "Botulinum toxin treatment of "one and a half syndrome"" (PDF). Br J ... There have been cases of improvement in extra-ocular movement with botulinum toxin injection. Internuclear ophthalmoplegia Wall ...
2007). Therapeutic Uses of Botulinum Toxin. Totowa, N.J.: Humana Press. p. 155. ISBN 9781597452472.. ... Kreyden, Oliver Philip; Böni, Roland Emil; Burg, Günter (2002). Hyperhidrosis and Botulinum Toxin in Dermatology: 18 Tables. ...
Injections of botulinum toxin into the bladder is another option. Urinary catheters or surgery are generally not recommended. A ... Botulinum toxin A (Botox) is approved by the Food and Drug Administration in adults with neurological conditions, including ... Botulinum Toxin A injections into the bladder wall can suppress involuntary bladder contractions by blocking nerve signals and ... ISBN 978-3-642-03579-1. Sacco E, Paolillo M, Totaro A, Pinto F, Volpe A, Gardi M, Bassi PF (2008). "Botulinum toxin in the ...
Injections of botulinum toxin type A can be used to block neural control of sweat glands. The effect can last from 3-9 months ... Comite SL, Smith K. "Commenting on: "Duration of efficacy increases with the repetition of botulinum toxin A injections in ... "Botulinum toxin in primary care medicine". The Journal of the American Osteopathic Association. 106 (10): 609-14. PMID 17122031 ... Percutaneous sympathectomy is a minimally invasive procedure similar to the botulinum method, in which nerves are blocked by an ...
Hodge, James G. "Botulinum Toxin". jhsph.edu. Johns Hopkins Center for Public Health Preparedness. Retrieved 4 August 2015. ...
2007). Therapeutic Uses of Botulinum Toxin. Totowa, N.J.: Humana Press. p. 155. ISBN 9781597452472. Böni, R.; Groscurth, P. ( ... Hyperhidrosis and Botulinum Toxin in Dermatology: 18 Tables. Karger Publishers. p. 8. ISBN 3805573065. Wilke et al. 2007, p. ...
Botulinum Toxin. http://www.sciencedirect.com/topics/neuroscience/hanatoxin. ... channel toxin known as δ-TLTX-Ta1a according to the currently developing systematic nomenclature for peptide and protein toxins ...
"Botulinum Toxin in Management of Limb Tremor". Toxins. 9 (11). doi:10.3390/toxins9110365. PMC 5705980. PMID 29125566.. ... When medications do not control the tremor or the person does not tolerate medication, botulinum toxin,[49][50][51][52] deep ... Samotus O, Kumar N, Rizek P, Jog M (January 2018). "Botulinum Toxin Type A Injections as Monotherapy for Upper Limb Essential ... "Long-term tremor therapy for Parkinson and essential tremor with sensor-guided botulinum toxin type A injections". PLOS One. 12 ...
Botulinum toxin solution ("Botox") is sometimes used to treat TMD.[73] Injection of botox into the lateral pterygoid muscle has ... Botulinum toxin causes temporary muscular paralysis by inhibiting acetylcholine release at the neuromuscular junction.[26] The ... Schwartz M, Freund B (Nov-Dec 2002). "Treatment of temporomandibular disorders with botulinum toxin". The Clinical Journal of ... "An evidence-based review of botulinum toxin (Botox) applications in non-cosmetic head and neck conditions". JRSM Short Reports ...
Botulinum toxin paralysis reduces total muscle force by removing, or reducing, the contractile component. Botulinum toxin is a ... Botulinum toxin has also been used intraoperatively to augment a surgical effect. In complex strabismus cases, toxin can be ... Botulinum A toxin (introduced as Oculinum, now called Botox, is the principal drug used to temporarily paralyze extraocular ... Botulinum toxin injection is commonly used for small and moderate degrees of infantile esotropia, acquired adult strabismus, ...
Botulinum toxin in ophthalmic plastic surgery. Indian J Ophthalmol. 2005;53:279-88. 132. Gupta R, Honavar SG, Vemuganti GK. ... Anterior chemodenervation of levator palpebrae superioris with botulinum toxin type-A Botox(R) to induce temporary ptosis for ...
See for example "Botulinum Toxin as a Biological Weapon". Dustiness is defined as the tendency of a powder material to generate ... "Botulinum Toxin as a Biological Weapon". Center For Infectious Disease Research & Policy. Yaobo Ding, Burkhard Stahlmecke, ...
Botulinum toxin therapy of strabismus. Medical imaging. *Fluorescein angiography. *Fundus photography. *Corneal topography ...
Botulinum toxin produced by Clostridium botulinum is the cause of botulism.[17] Humans most commonly ingest the toxin from ... Botulinum toxin A is marketed under the brand names Jeuveau, Botox and Xeomin. Botulinum toxin B is marketed under the brand ... when samples containing botulinum toxin are tested.[citation needed] To confirm a diagnosis of botulinum toxin poisoning, ... botulinum toxin is being evaluated for use in treating chronic pain.[39] Studies show that botulinum toxin may be injected into ...
Botulinum toxin is used to treat a number of problems. Muscle spasticity[edit]. Botulinum toxin is used to treat a number of ... Botulinum toxin produced by Clostridium botulinum is the cause of botulism.[9] Humans most commonly ingest the toxin from ... Botulinum toxin A is marketed under the brand names Botox and Xeomin. Botulinum toxin B is marketed under the brand name ... when samples containing botulinum toxin are tested.[citation needed] To confirm a diagnosis of botulinum toxin poisoning, ...
Clostridium botulinum.,/I, The toxins are proteins with molecular weights of approximately 150,000, which bind to the ... The toxin is also a popular agent for its cosmetic uses. Botulinum toxins as a Biological Weapon. Botulinum toxins have been ... Botulinum Toxins. Botulinum Toxins are produced by the bacteria Clostridium botulinum under anaerobic conditions. The bacteria ... Botulinum toxins are some of the most lethal known toxins. The toxin blocks the nerves ability to release acetylcholine, the ...
Botulinum toxin.. BMJ 1992; 305 doi: https://doi.org/10.1136/bmj.305.6863.1169 (Published 14 November 1992) Cite this as: BMJ ...
Botulinum toxin. BMJ 1989; 298 doi: https://doi.org/10.1136/bmj.298.6672.522-b (Published 25 February 1989) Cite this as: BMJ ...
... is produced by Clostridium botulinum, a gram-positive anaerobic bacterium.{ref1} The clinical syndrome of botulism can occur ... Botulinum toxin (abbreviated either as BTX or BoNT) ... Botulinum Toxin Q&A What is botulinum toxin (BoNT)?. Updated: ... encoded search term (What is botulinum toxin (BoNT)?) and What is botulinum toxin (BoNT)? What to Read Next on Medscape. ... Botulinum toxin (abbreviated either as BTX or BoNT) is produced by Clostridium botulinum, a gram-positive anaerobic bacterium. ...
Botulinum Toxin (Botox) for Facial Wrinkles (American Academy of Ophthalmology) * Botulinum Toxin Injections: A Treatment for ... Botox is a drug made from a toxin produced by the bacterium Clostridium botulinum. Its the same toxin that causes a life- ... Botulinum Toxin Therapy: Overview (American Academy of Dermatology) * Can Botox Injections Relieve Arthritis Pain? (Mayo ... Article: Calcitonin gene-related peptide antagonists versus botulinum toxin A for the preventive... ...
This primer covers the various preparations of botulinum toxin and their safe use for cosmetic and functional indications in ... and potential complications of botulinum toxin.. Several preparations of botulinum toxin have emerged over the past decade. The ... Table 1. Type A Botulinum Toxins Available for Therapeutic Injection in the United States Toxins. Trade Name. Manufacturer. ... Indeed, injection of botulinum toxin is now the most frequently performed nonsurgical cosmetic procedure.[4] Given its ...
Botulinum toxin type A that is free of complexing proteins found in natural toxin from Clostridium botulinum. Acetylcholine ... Botulinum toxin in blepharospasm and oromandibular dystonia: comparing different botulinum toxin preparations. Eur J Neurol. ... The use of botulinum toxin type-B in the treatment of patients who have become unresponsive to botulinum toxin type-A -- ... Unlabeled uses of botulinum toxins: a review, part 2. Am J Health Syst Pharm. 2006 Feb 1. 63(3):225-32. [Medline]. ...
Botulinum neurotoxin (BoNT) produced by Clostridium botulinumis the most toxic substance known to humans that causes the ... Botulinum Toxin Cervical Dystonia Botulinum Neurotoxin Clostridium Botulinum Neurogenic Detrusor Overactivity These keywords ... Immunogenecity of botulinum toxins. J Neural Transm. 2013;120:275-90.CrossRefPubMedPubMedCentralGoogle Scholar ... A self-pumping lab-on-a-chip for rapid detection of botulinum toxin. Lab Chip. 2010;10:2265-70.CrossRefPubMedGoogle Scholar ...
Botulimum toxin (BTX) is a type of nerve blocker. When injected, BTX blocks nerve signals to muscles so they relax. ... guided botulinum toxin treatment; Percutaneous indirect laryngoscopy - guided botulinum toxin treatment; Adductor dysphonia-BTX ... BTX is the toxin that causes botulism, a rare but serious illness. It is safe when used in very small doses. ... Botulimum toxin (BTX) is a type of nerve blocker. When injected, BTX blocks nerve signals to muscles so they relax. ...
Nobre M.E., Ciciarelli M.C., Souza J.A. (2019) Botulinum Toxin for Migraine. In: Issa M., Tamura B. (eds) Botulinum Toxins, ... Botulinum toxin type A (BTX-A) for migraine: an open label assessment. Mov Disord. 1998b;13:241. (Abstract)Google Scholar ... Treatment of hyperfunctional lines of the face with botulinum toxin A. Dermatol Surg. 1998a;24:1198-205.PubMedGoogle Scholar ... Botulinum toxin type A versus amitriptyline for the treatment of chronic daily migraine. Clin Neurol Neurosurg. 2010;112:463-6. ...
... which is a toxin produced by the bacteria Clostridium botulinum. ... injections contain the active ingredient botulinum toxin type A ... Vistabel (Botulinum toxin type A). Vistabel injections contain the active ingredient botulinum toxin type A, which is a toxin ... which is a toxin produced by the bacteria Clostridium botulinum.. Botulinum toxin type A is a bacterial toxin that prevents ... Tell your doctor if you have recently had any other botulinum toxin injections, because if this injection is given too close to ...
... This must be done with great care to avoid paralysing nearby muscle groups with resulting ... My consultant now wants to try botulinum toxin injections. I think I am right in saying that these will weaken my muscles and ... The botulinum toxin is injected by the specialist to deliberately paralyse the muscles that are causing the spasms. ... Please tell me about botulinum toxin. For three years I have suffered from spinal myoclonus, which mainly causes frequent and ...
Long-Term Outcome of Patients With Intractable Chronic Cluster Headache Treated With Injection of Onabotulinum Toxin A Toward ...
Diffusion, spread, and migration of botulinum toxin.. Ramirez-Castaneda J1, Jankovic J, Comella C, Dashtipour K, Fernandez HH, ... Botulinum toxin (BoNT) is an acetylcholine release inhibitor and a neuromuscular blocking agent used for the treatment of a ... The passive kinetic dispersion of the toxin away from the injection site in a gradient-dependent manner may also play a role in ... toxin spread. In addition to unique properties of the various BoNT products, volume and dilution may also influence local and ...
This article presents a pathophysiological rationale for dual therapy with anti-CGRP humanized antibodies and botulinum toxin ... Dual Therapy With Anti-CGRP Monoclonal Antibodies and Botulinum Toxin for Migraine Prevention. Is There a Rationale?. ... Results: Preclinical data suggest that anti-calcitonin gene-related peptide monoclonal antibodies and botulinum toxin type A ... Headache guidelines recommend several pharmacological therapies, including oral medications, botulinum toxin type A (BTX-A), ...
Botulinum toxin is an injectable neuromodulator derived from neurotoxins produced byClostridium botulinum, the bacterium ... Botulinum toxin type B (MYOBLOC) versus botulinum toxin type A (BOTOX) frontalis study: rate of onset and radius of diffusion. ... The use of botulinum toxin for specific cosmetic or medical indications is discussed elsewhere. (See Botulinum toxin for ... Botulinum toxin type B for dynamic glabellar rhytides refractory to botulinum toxin type A. Dermatol Surg 2003; 29:516. ...
Injecting botulinum toxin into the fat pads around the heart after bypass surgery might stave off postoperative atrial ... "If, in fact, at the time of surgery you can squirt some [botulinum toxin] into the four fat pads, and if that is quick and safe ... Calkins said hes not sure what botulinum toxin costs, but "if it adds 5 minutes to surgery and its safe and it adds $200 to ... SAN FRANCISCO -- Injecting botulinum toxin into the fat pads around the heart after bypass surgery might stave off ...
Helping you find trustworthy answers on Botulinum Toxin Injection , Latest evidence made easy ... Find all the evidence you need on Botulinum Toxin Injection via the Trip Database. ... 2. Toxins for Health? Botulinum toxin for migraine for Health? Botulinum toxin for migraine. Clinical Question: What is the ... Injection of botulinum toxin (Botox) for prophylaxis of headaches in adults with chronic migraine Injection of botulinum toxin ...
... , Onabotulinum Toxin A, Abobotulinum Toxin A, Botulinum Toxin Type A, Botox. ... botulinum injection toxin, botulinum injections toxin, injection of botulinum toxin, botulinum toxin injection, Botulinum toxin ... Botulinum Toxin Injection. Botulinum Toxin Injection Aka: Botulinum Toxin Injection, Onabotulinum Toxin A, Abobotulinum Toxin A ... Botulinum Toxin serotype A (most common serotype used for cosmetic procedures). *Onabotulinum Toxin A (Botox) ...
Distant effects of local injection of botulinum toxin.. Lange DJ, Brin MF, Warner CL, Fahn S, Lovelace RE. ... We studied five patients who received local injections of botulinum toxin for dystonic disorders to determine if there had been ... In all patients who received more than 245 U of toxin, SFEMG in the extensor digitorum communis muscle, a muscle distant to all ... results reveal that there is an effect on neuromuscular transmission in muscles distant to those injected with botulinum toxin ...
Combining hyaluronic acid fillers and botulinum toxin provides reflation and relaxation of the lower face and perioral region, ... "If you combine [botulinum toxin] with [hyaluronic acid], there is longer viability of the filler, and it makes sense because ... "In the old days, there was a lot of concern that the use of [botulinum toxin] in the lower face would cause distortion or ... "The side effects you tend to see with [botulinum toxin] around the lips - the potential slurring of words, drooling, or some ...
Nonaesthetic Applications for Botulinum Toxin in Plastic Surgery * Botulinum Toxin Reduces Chronic Pelvic Pain in Endometriosis ... Botulinum toxin for blepharospasm. Jankovic J, Hallett M, eds. Therapy with Botulinum Toxin. New York: Marcel Dekker; 1994. 299 ... encoded search term (Dystonia Treatment using Botulinum Toxin) and Dystonia Treatment using Botulinum Toxin What to Read Next ... Botulinum toxin treatment of focal hand dystonia. Jankovic J, Hallett M, eds. Therapy with Botulinum Toxin. New York: Marcel ...
... is raising questions about the therapeutic use of botulinum toxin A. The study found that animals injected with Clostridium ... Botulinum Toxin A is also used as a cosmetic treatment, where the drug paralyzes small muscles in the face to reduce the ... "We were surprised by the degree of muscle loss and atrophy in the limb that was not injected with the Botulinum toxin," says ... This study shows, for the first time, that over time Botulinum toxin A use also results in muscle weakness, atrophy and loss of ...
  • These conditions are listed below: Perinatal (during birth) cerebral injury Kernicterus Cerebrovascular diseases Drug induced Central nervous system tumor Peripheral or central trauma Infectious or post infectious encephalopathies Toxins Metabolic Paraneoplastic syndromes Central pontine myelinolysis Secondary spasmodic torticollis is diagnosed when any of the following are present: history of exogenous insult or exposure, neurological abnormalities other than dystonia, abnormalities on brain imaging, particularly in the basal ganglia. (wikipedia.org)
  • Following this voluntary admission, the 1995 defection and debriefing of a key Iraqi official provided western intelligence experts with evidence of 100 R400 bombs and 13 Al Hussein SCUDS that were loaded with 19,000 liters of concentrated botulinum toxins. (globalsecurity.org)
  • Functional repair of motor endplates after botulinum neurotoxin type A poisoning: biphasic switch of synaptic activity between nerve sprouts and their parent terminals. (medscape.com)
  • Attrée O, Guglielmo-Viret V, Gros V, Thullier P. Development and comparison of two immunoassay formats for rapid detection of botulinum neurotoxin type A. J Immunol Methods. (springer.com)
  • At the same time, botulinum neurotoxin type A1 is successfully used to treat a variety of human syndromes characterized by hyperactive cholinergic nerve terminals. (mdpi.com)
  • This review provides updated information about the effect of botulinum toxin injection on local pain caused by cancer, painful muscle spasms from a remote cancer, and pain at the site of cancer surgery and radiation. (mdpi.com)
  • Before physicians started getting creative with the products, botulinum toxin was primarily used in the upper face to treat the glabella and periorbital wrinkles, whereas the lower face and perioral region were primarily treated with fillers, according to Gary D. Monheit, MD, lead author of the study and associate clinical professor in the Departments of Dermatology and Ophthalmology at the University of Alabama in Birmingham. (medscape.com)
  • Thinking about getting botulinum toxin injections for wrinkles? (aao.org)
  • They can use Botulinum toxin to prevent wrinkles and get face lifts. (wikipedia.org)