botulism/بوتاسيوم

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Botulism as a sequel to open castration in a horse.

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Clostridium botulinum and type-B C botulinum toxin were isolated from a necrotic wound that developed subsequent to castration in a 2-year-old Thoroughbred gelding. The horse had clinical signs of botulism and was successfully treated with wound debridement, C botulinum type-B antitoxin, potassium

Elucidating the molecular basis of action of a classic drug: guanidine compounds as inhibitors of voltage-gated potassium channels.

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Guanidine and its alkyl analogs stimulate the neuromuscular junction presynaptically by inhibiting voltage-gated potassium (Kv) channels, leading to enhanced release of acetylcholine in the synaptic cleft. This stimulatory effect of guanidine underlies its use in the therapy for the neuromuscular

The anti-botulism triterpenoid toosendanin elicits calcium increase and exocytosis in rat sensory neurons.

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Toosendanin, a triterpenoid from Melia toosendan Sieb et Zucc, has been found before to be an effective anti-botulism agent, with a bi-phasic effect at both motor nerve endings and central synapse: an initial facilitation followed by prolonged depression. Initial facilitation may be due to

Symptomatic treatment of botulism with a clinically approved small molecule.

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Botulinum neurotoxins (BoNTs) are potent neuroparalytic toxins that cause mortality through respiratory paralysis. The approved medical countermeasure for BoNT poisoning is infusion of antitoxin immunoglobulins. However, antitoxins have poor therapeutic efficacy in symptomatic patients; thus, there

[Mechanism of the change in electrolyte and carbohydrate metabolism in the submandibular salivary gland in experimental botulism in rats].

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Content of lactic and pyruvic acids, glycogen, sodium and potassium ions are well as the total LDH activity and its isoenzyme spectrum were not distinctly altered, when secretion of salivary glands was inhibited by administration of botulinic toxin into rats (within 48 hrs after the toxin

Acute Neuromuscular Disorders in the Pediatric Intensive Care Unit.

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The neuromuscular disorders encountered in the pediatric intensive care unit (PICU) encompass a broad spectrum of pathologies. These include acute disorders (eg, Guillain-Barre syndrome), acute-on-chronic disorders (eg, myasthenia gravis), progressive disorders (eg, muscular

Neuropathogenic properties of Argas (Persicargas) walkerae larval homogenates.

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Several tick species have been demonstrated, described, or suspected to cause paralysis in their host during the repletion process, presumably by impairing neurotransmission. The resulting polyneuropathy gradually spreads to the upper limbs causing incoordination and ends in respiratory failure.

3,4-diaminopyridine reverses paralysis in botulinum neurotoxin-intoxicated diaphragms through two functionally distinct mechanisms.

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Botulinum neurotoxins (BoNTs) are exceedingly potent neurological poisons that prevent neurotransmitter release from peripheral nerve terminals by cleaving presynaptic proteins required for synaptic vesicle fusion. The ensuing neuromuscular paralysis causes death by asphyxiation. Although no

[Role of hypoxia factor in changes of ionic composition of blood and muscle tissue in experimental botulinum poisoning].

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Levels of sodium and potassium ions in muscle tissue, blood plasma and red cells were measured, and the index characterizing the capacity of tissue to accumulate cations from the environment and the discrimination coefficient were calculated in experiments on white rats subjected to experimental

Formulating a new basis for the treatment against botulinum neurotoxin intoxication: 3,4-Diaminopyridine prodrug design and characterization.

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Botulism is a disease characterized by neuromuscular paralysis and is produced from botulinum neurotoxins (BoNTs) found within the Gram positive bacterium Clostridium botulinum. This bacteria produces the most deadliest toxin known, with lethal doses as low as 1 ng/kg. Due to the relative ease of

4-aminopyridine-a review.

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4-aminopyridine is the first of the aminopyridines to be used in clinical practice. It blocks potassium channels and thereby increases acetylcholine, and possibly noradrenaline, release at nerve terminals. In man the drug has a significant action at the neuromuscular junction, but has little effect

[Ptosis in the differential diagnosis of neurologic diseases].

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This review summarizes those neurological diseases which are accompanied by a drooping of the upper lid, due to weakness of the m. levator palpebrae or m. tarsalis respectively. After connatal ptosis with or without involvement of other bulbar muscles the different types of muscular dystrophies are

Symptomatic relief of botulinum neurotoxin/a intoxication with aminopyridines: a new twist on an old molecule.

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Botulinum neurotoxins (BoNT) are the etiological agents responsible for botulism, a disease characterized by peripheral neuromuscular blockade and a characteristic flaccid paralysis of humans. BoNT/A is the most toxic protein known to man and has been classified by the Centers of Disease Control

Approach to generalized weakness and peripheral neuromuscular disease.

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A large number of intellectually engaging and potentially serious neuromuscular diseases have been presented. The emergency medicine physician must be able to recognize those entities that have the potential to clinically deterioration. The evaluation of weakness requires a comprehensive,

In vitro characterization of botulinum toxin types A, C and D action on human tissues: combined electrophysiologic, pharmacologic and molecular biologic approaches.

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Human exposure to botulinum toxin typically occurs in two settings: 1) as an etiologic agent in the disease botulism and 2) as a therapeutic agent for the treatment of dystonia. Epidemiologic studies on botulism suggest that the human nervous system is susceptible to five toxin serotypes (A, B, E, F

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