Search results for "botulinum"

showing 10 items of 84 documents

Differences in the temperature dependencies of uptake of botulinum and tetanus toxins in Aplysia neurons

1992

The respective neuroselective actions of botulinum type A (BoNT) and tetanus (TeTx) neurotoxins on cholinergic and non-cholinergic synapses of Aplysia are mainly due to differences in their extracellular neuronal targetting. Further information was gained on this neuroselectivity by examining the temperature dependencies of binding, internalization and intracellular action of both toxins. After reduction of temperature from 22 degrees C to 10 degrees C, the binding of neither BoNT nor TeTx was significantly altered whereas the neuronal uptake of BoNT, but not of TeTx, was prevented. Although TeTx internalization could be detected at the low temperature, its intracellular activity was greatl…

NeuronsBotulinum ToxinsGeneral Neurosciencemedia_common.quotation_subjectTemperatureBiologybiology.organism_classificationAcetylcholineSynapseTetanus ToxinAplysiaAplysiamedicineExtracellularBiophysicsAnimalsNeurotoxinCholinergicInternalizationNeuroscienceAcetylcholineIntracellularmedia_commonmedicine.drugNeuroscience Letters
researchProduct

A role for Rho in receptor- and G protein-stimulated phospholipase C Reduction in phosphatidylinositol 4,5-bisphosphate by Clostridium difficile toxi…

1996

Receptors coupled to heterotrimeric guanine nucleotide-binding proteins (G proteins) activate phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2)-hydrolyzing phospholipase C (PLC) enzymes by activated alpha of free beta gamma subunits of the relevant G proteins. To study whether low molecular weight G proteins of the Rho family are involved in receptor signaling to PLC, we examined the effect of Clostridium difficile toxin B, which glucosylates and thereby inactivates Rho proteins, on the regulation of PLC activity in human embryonic kidney (HEK) cells stably expressing the m3 muscarinic acetylcholine receptor (mAChR) subtype. Toxin B treatment of HEK cells did not affect basal PLC activi…

Phosphatidylinositol 45-DiphosphateBotulinum ToxinsG proteinBacterial ToxinsClostridium difficile toxin AClostridium difficile toxin BBiologychemistry.chemical_compoundBacterial ProteinsGTP-Binding ProteinsHeterotrimeric G proteinHumansPhosphatidylinositolCells CulturedADP Ribose TransferasesPharmacologyPhospholipase CHEK 293 cellsGeneral MedicineReceptors MuscarinicMolecular biologyCell biologychemistryPhosphatidylinositol 45-bisphosphateType C PhospholipasesrhoA GTP-Binding ProteinNaunyn-Schmiedeberg's Archives of Pharmacology
researchProduct

Inhibition of Receptor Signaling to Phospholipase D by Clostridium difficile Toxin B

1996

Rho proteins have been reported to activate phospholipase D (PLD) in in vitro preparations. To examine the role of Rho proteins in receptor signaling to PLD, we studied the effect of Clostridium difficile toxin B, which glucosylates Rho proteins, on the regulation of PLD activity in human embryonic kidney (HEK) cells stably expressing the m3 muscarinic acetylcholine receptor (mAChR). Toxin B treatment of HEK cells potently and efficiently blocked mAChR-stimulated PLD. In contrast, basal and phorbol ester-stimulated PLD activities were not or only slightly reduced. Cytochalasin B and Clostridium botulinum C2 toxin, mimicking the effect of toxin B on the actin cytoskeleton but without involvi…

Phospholipase DG proteinClostridium difficile toxin AClostridium difficile toxin BCell BiologyBiologymedicine.disease_causeActin cytoskeletonBiochemistryMolecular biologyenzymes and coenzymes (carbohydrates)chemistry.chemical_compoundchemistrymedicineClostridium botulinumlipids (amino acids peptides and proteins)Signal transductionMolecular BiologyCytochalasin BJournal of Biological Chemistry
researchProduct

Botulinum A and the light chain of tetanus toxins inhibit distinct stages of Mg.ATP-dependent catecholamine exocytosis from permeabilised chromaffin …

1994

Susceptibilities of Mg.ATP-independent and Mg.ATP-requiring components of catecholamine secretion from digitonin-permeabilised chromaffin cells to inhibition by Clostridial botulinum type A and tetanus toxins were investigated. These toxins are Zn(2+)-dependent proteases which specifically cleave the 25-kDa synaptosomal-associated protein (SNAP-25) and vesicle-associated membrane protein (VAMP) II, respectively. When applied to permeabilised chromaffin cells they rapidly inhibited secretion in the presence of Mg.ATP but the catecholamine released in the absence of Mg.ATP, thought to represent fusion of primed granules, was not perturbed. The toxins can exert their effects per se in the abse…

ProteasesBotulinum ToxinsCell Membrane PermeabilityBiologymedicine.disease_causeBiochemistryExocytosisExocytosischemistry.chemical_compoundAdenosine TriphosphateCatecholaminesTetanus ToxinmedicineAnimalsSecretionChromaffin GranulesCells CulturedToxinKineticsmedicine.anatomical_structurechemistryMembrane proteinBiochemistryAdrenal MedullaCatecholamineCattleAdrenal medullaAdenosine triphosphatemedicine.drugEuropean journal of biochemistry
researchProduct

Processing of tetanus and botulinum A neurotoxins in isolated chromaffin cells.

1995

Tetanus and botulinum A neurotoxins were introduced into the cytosol of chromaffin cells by means of an electric field in which the plasma membrane is forced to form pores of approximately 1 micron at the sites facing the electrodes. As demonstrated by electron microscopy, both [125I] and gold-labelled tetanus toxin (TeTx) diffuse through these transient openings. Dichain-TeTx, with its light chain linked to the heavy chain by means of a disulfide bond, causes the block of exocytosis to develop more slowly than does the purified light chain. The disulfide bonds, which in both toxins hold the subunits together, were cleaved by the intrinsic thioredoxin-reductase system. Single chain TeTx, in…

ProteasesBotulinum ToxinsCell Membrane PermeabilityProteolysisImmunoglobulin light chainmedicine.disease_causeExocytosisExocytosisTetanus ToxinmedicinePeptide bondAnimalsCells CulturedPharmacologymedicine.diagnostic_testToxinChemistryGeneral MedicineCytosolMicroscopy ElectronElectroporationBiochemistryAdrenal MedullaBiophysicsMicroscopy Electron ScanningCattleIntracellularNaunyn-Schmiedeberg's archives of pharmacology
researchProduct

Inhibition in vivo of the activity of botulinum neurotoxin A by small molecules selected by virtual screening

2012

To search for small molecular size inhibitors of botulinum neurotoxin A (BoNT/A) endopeptidase activity, we have screened the NCI library containing about 1 million structures against the substrate binding pocket of BoNT/A. Virtual screening (VS) was performed with the software Glide (Grid-based ligand docking energetics) and the findings were confirmed by AutoDock. Ten compounds were found that had favorable energetic and glide criteria and 5 of these compounds were selected for their ability to protect mice in vivo against a lethal dose of BoNT/A. Each compound was incubated at different molar excesses with a lethal dose of the toxin and then the mixture injected intravenously into mice. …

Protein ConformationToxinChemistryNeurotoxinsLethal doseComputational BiologyAutoDockPharmacologyProtective AgentsToxicologymedicine.disease_causeSmall moleculeToxicologyMiceEndopeptidase activityDocking (molecular)In vivoToxicitymedicineAnimalsBotulinum Toxins Type ASequence AlignmentSoftwareToxicon
researchProduct

Repeated pull-through surgery for complicated Hirschsprung's disease--principles derived from clinical experience.

2007

Abstract Background In some patients, an initial pull-through procedure for Hirschsprung's disease fails, and obstructive symptoms persist or recur. Then a repeated pull-through operation may be necessary. Methods Seventeen patients with Hirschsprung's disease aged 2 to 9 years (median, 4.6 years) have undergone a repeated pull-through procedure because of unresponsive symptoms after an initial operation. The initial procedure was Soave in 3 patients, Rehbein in 13 patients, and Duhamel in 1 patient. Surgical revision was indicated by incomplete resection of the transition zone in 16 patients, anastomotic strictures in 9 patients, and fistulas in 2 patients. All 17 patients have undergone R…

Reoperationmedicine.medical_specialtyConstipationScarsAnastomosismedicineHumansHirschsprung DiseaseChildHirschsprung's diseasePelvisDigestive System Surgical Proceduresbusiness.industryGeneral MedicineIncomplete Resectionmedicine.diseaseBotulinum toxinSurgerymedicine.anatomical_structureChild PreschoolPediatrics Perinatology and Child HealthCuffSurgerymedicine.symptombusinessIntestinal Obstructionmedicine.drugJournal of pediatric surgery
researchProduct

Botulinum toxin in preparation of oral cavity for microsurgical reconstruction.

2010

CONCLUSIONS: Infiltration of botulinum toxin in the major salivary glands allows a temporary reduction of salivation that begins 8 days afterwards and returns to normal within 2 months. The inhibition of salivary secretion, carried out before the oral cavity reconstructive surgery, could allow a reduction of the incidence of oro-cutaneous fistulas and local complications. OBJECTIVES: Saliva stagnation is a risk factor for patients who have to undergo reconstructive microsurgery of the oral cavity, because of fistula formation and local complications in the oral cavity. The authors suggest infiltration of botulinum toxin in the major salivary glands to reduce salivation temporarily during th…

SalivaReconstructive surgerymedicine.medical_specialtyMicrosurgeryBotulinum Toxins Type A/administration & dosage* Humans Microsurgery* Mouth Floor/surgery Mouth Neoplasms/surgery* Neck Dissection Neoplasm Invasiveness Preoperative Care* Salivary Glands/drug effects* Salivation/drug effects Surgical Flaps Tongue Neoplasms/surgeryFistulamedicine.medical_treatmentSalivary GlandsSurgical FlapsMajor Salivary GlandPreoperative CareMedicineHumansOral Cavity CarcinomaNeoplasm InvasivenessBotulinum Toxins Type AMouth Floorbusiness.industryGeneral MedicineMicrosurgerymedicine.diseaseBotulinum toxinSurgeryTongue NeoplasmsOtorhinolaryngologyNeck DissectionMouth NeoplasmsbusinessComplicationSalivationmedicine.drugActa oto-laryngologica
researchProduct

Inhibition of FcεRI-mediated Activation of Rat Basophilic Leukemia Cells by Clostridium difficile Toxin B (Monoglucosyltransferase)

1996

Abstract Treatment of rat basophilic leukemia (RBL) 2H3-hm1 cells with Clostridium difficile toxin B (2 ng/ml), which reportedly depolymerizes the actin cytoskeleton, blocked [3H]serotonin release induced by 2,4-dinitrophenyl-bovine serum albumin, carbachol, mastoparan, and reduced ionophore A23187-stimulated degranulation by about 55-60%. In lysates of RBL cells, toxin B 14C-glucosylated two major and one minor protein. By using two-dimensional gel electrophoresis and immunoblotting, RhoA and Cdc42 were identified as protein substrates of toxin B. In contrast to toxin B, Clostridium botulinum transferase C3 that selectively inactivates RhoA by ADP-ribosylation did not inhibit degranulation…

SerotoninRHOABacterial ToxinsClostridium difficile toxin AWasp VenomsClostridium difficile toxin BBiologyCytoplasmic GranulesTritiummedicine.disease_causeBiochemistryCell LinePhosphatidylinositol 3-KinasesBacterial ProteinsTumor Cells CulturedmedicineAnimalsEnzyme InhibitorsMolecular BiologyCalcimycinAdenosine Diphosphate RiboseClostridioides difficileReceptors IgEToxinDegranulationSerum Albumin BovineCell BiologyActin cytoskeletonMolecular biologyRatsAndrostadienesKineticsPhosphotransferases (Alcohol Group Acceptor)Leukemia Basophilic AcuteBiochemistryGlucosyltransferasesMastoparanbiology.proteinIntercellular Signaling Peptides and ProteinsClostridium botulinumCarbacholCattle24-DinitrophenolPeptidesWortmanninDinitrophenolsJournal of Biological Chemistry
researchProduct

Botulinum Toxin Is Effective in the Management of Neurogenic Dysphagia. Clinical-Electrophysiological Findings and Tips on Safety in Different Neurol…

2017

Background and Aims: Neurogenic dysphagia linked to failed relaxation of the upper esophageal sphincter (UES) can be treated by injecting botulinum toxin (BTX) into the cricopharyngeal (CP) muscle. We compared the effects of this treatment in different neurological disorders with dysphagia, to evaluate its efficacy over time including the response to a second injection. Materials and Methods: Sixty-seven patients with neurogenic dysphagia associated with incomplete or absent opening of the UES (24 with brainstem or hemispheric stroke, 21 with parkinsonian syndromes, 12 with multiple sclerosis, and 10 with spastic-dystonic syndromes secondary to post-traumatic encephalopathy) were treated wi…

Side effectEncephalopathyupper esophageal sphincter dysmotilityneurogenic dysphagia03 medical and health sciences0302 clinical medicineSwallowingmedicineIngestionPharmacology (medical)botulinum toxinOriginal ResearchPharmacologybusiness.industryelectrophysiological study of swallowingMultiple sclerosiscricopharyngeal musclemedicine.diseaseDysphagiaBotulinum toxinPneumoniaAnesthesia030211 gastroenterology & hepatologymedicine.symptombusiness030217 neurology & neurosurgerymedicine.drugFrontiers in Pharmacology
researchProduct