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botulism/carbohydrate
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[The role of the nervous system in the mechanism of breakdown of carbohydrate and energy metabolism in muscle tissue under experimental botulism].
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In skeletal muscle under a local botulinic intoxication and denervation the alterations in metabolism of glycogen, phosphocreatine, lactic and pyruvic acids were studied. The data obtained suggest that the dissimilarity in impairments of carbohydrate-energy metabolism in botulism and denervation was
[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
Inhibiting oral intoxication of botulinum neurotoxin A complex by carbohydrate receptor mimics.
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Botulinum neurotoxins (BoNTs) cause the disease botulism manifested by flaccid paralysis that could be fatal to humans and animals. Oral ingestion of the toxin with contaminated food is one of the most common routes for botulism. BoNT assembles with several auxiliary proteins to survive in the
Quantitative effects of carbohydrates and aromatic amino acids on Clostridium botulinum toxin gene expression using a rapid competitive RT/PCR assay.
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A rapid competitive RT/PCR assay was developed to determine the effects of nutrients on Clostridium botulinum type E toxin gene expression. The type E strain (EVH) was grown in a nutrient-rich broth containing 1% glucose (base medium). Toxin gene expression was quantified at both mid and late
Functional dissection of the Clostridium botulinum type B hemagglutinin complex: identification of the carbohydrate and E-cadherin binding sites.
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Botulinum neurotoxin (BoNT) inhibits neurotransmitter release in motor nerve endings, causing botulism, a condition often resulting from ingestion of the toxin or toxin-producing bacteria. BoNTs are always produced as large protein complexes by associating with a non-toxic protein, non-toxic
Structural analysis by X-ray crystallography and calorimetry of a haemagglutinin component (HA1) of the progenitor toxin from Clostridium botulinum.
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Botulism food poisoning is caused primarily by ingestion of the Clostridium botulinum neurotoxin (BoNT). The 1300 amino acid BoNT forms a progenitor toxin (PTX) that, when associated with a number of other proteins, increases its oral toxicity by protecting it from the low pH of the stomach and from
Fatal Clostridium botulinum toxicosis in eleven Holstein cattle fed round bale barley haylage.
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Twenty-two lactating Holstein cattle in Tennessee had clinical signs of intoxication with preformed Clostridium botulinum toxin. These signs included weakness, paralysis of the tongue and chest muscles, abdominal breathing, and, in 11 of the 22 cows, death. Differential diagnoses included
Insights into the Mechanisms by Which Clostridial Neurotoxins Discriminate between Gangliosides.
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Botulinum neurotoxins (BoNTs) and tetanus neurotoxin (TeNT) are the causative agents of the paralytic diseases botulism and tetanus, respectively. Entry of toxins into neurons is mediated through initial interactions with gangliosides, followed by binding to a protein co-receptor. Herein, we aimed
Human milk SIgA binds to botulinum type B 16S toxin and limits toxin adherence on T84 cells.
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Botulinum neurotoxin produced by Clostridium botulinum type B is in the form of a complex of 12S and 16S toxins. Food-borne botulism is caused by these complex toxins which are ingested orally and absorbed from the digestive tract. Here, we show that the human milk SIgA binds to the type B16S toxin.
Type E Botulinum Neurotoxin-Producing Clostridium butyricum Strains Are Aerotolerant during Vegetative Growth.
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Clostridium butyricum, the type species of the genus Clostridium, is considered an obligate anaerobe, yet it has been shown to grow in the presence of oxygen. C. butyricum strains atypically producing the botulinum neurotoxin type E are the leading cause of type E human botulism in
Heat shock and prolonged heat stress attenuate neurotoxin and sporulation gene expression in group I Clostridium botulinum strain ATCC 3502.
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Foodborne pathogenic bacteria are exposed to a number of environmental stresses during food processing, storage, and preparation, and in the human body. In order to improve the safety of food, the understanding of molecular stress response mechanisms foodborne pathogens employ is essential. Many
High-resolution crystal structure of HA33 of botulinum neurotoxin type B progenitor toxin complex.
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Botulinum neurotoxins (BoNTs) are produced as progenitor toxin complexes (PTCs) by Clostridium botulinum. The PTCs are composed of BoNT and non-toxic neurotoxin-associated proteins (NAPs), which serve to protect and deliver BoNT through the gastrointestinal tract in food borne botulism. HA33 is a
Functional Analysis of Botulinum Hemagglutinin (HA).
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Botulinum neurotoxin (BoNT), produced by Clostridium botulinum, is the most potent toxin and produced as a complex with non-toxic components. Food-borne botulism is caused by the ingestion of these BoNT complexes. Hemagglutinin (HA), one of the non-toxic components, is known to have lectin
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,
Structure of a bimodular botulinum neurotoxin complex provides insights into its oral toxicity.
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Botulinum neurotoxins (BoNTs) are produced by Clostridium botulinum and cause the fatal disease botulism, a flaccid paralysis of the muscle. BoNTs are released together with several auxiliary proteins as progenitor toxin complexes (PTCs) to become highly potent oral poisons. Here, we report the
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