Search results for "neurotoxin"

showing 10 items of 53 documents

Treatment of masseteric hypertrophy with botulinum toxin: A report of two cases

2010

BAS, BURCU/0000-0003-0593-3400; Kutuk, Nukhet/0000-0001-6563-1899 WOS: 000279667400021 PubMed: 20173718 Masseter muscle hypertrophy is a rare condition of unknown cause which is important in the differential diagnosis of head and neck masses, located in the cheek. Several treatment options reported for masseter hypertrophy, which range from simple pharmacotherapy to more invasive surgical reduction. Botulinum toxin type A is a powerful neurotoxin which is produced by the anaerobic organism Clostridium botulinum and when injected into a muscle causes interference with the neurotransmitter mechanism producing selective paralysis and subsequent atrophy of the muscle. Injection of botulinum tox…

AdultMalemedicine.medical_specialtyNeurotoxinsmedicine.disease_causeMuscle hypertrophyMasseter muscleAtrophyParalysismedicineNeurotoxinHumansBotulinum Toxins Type AGeneral Dentistrybusiness.industryMasseter MuscleHypertrophyCheekmedicine.disease:CIENCIAS MÉDICAS [UNESCO]SurgeryMasseter musclebotulinum toxin type Amedicine.anatomical_structureOtorhinolaryngologyUNESCO::CIENCIAS MÉDICASClostridium botulinumSurgeryFemalemedicine.symptomDifferential diagnosisbusinesshypertrophy
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Impaired calcium homeostasis in aged hippocampal neurons

2009

Abstract Development of neurodegenerative diseases such as Alzheimer's and Parkinson's disease is strongly age-associated. The impairment of calcium homeostasis is considered to be a key pathological event leading to neuronal dysfunction and cell death. However, the exact impact of aging on calcium homeostasis in neurons remains largely unknown. In the present work we have investigated intracellular calcium levels in cultured primary hippocampal neurons from young (2 months) and aged (24 months) rat brains. Upon stimulation with glutamate or hydrogen peroxide aged neurons in comparison to young neurons demonstrated an increased vulnerability to these disease-related toxins. Measurement of c…

Agingmedicine.medical_specialtyNeurotoxinsGlutamic Acidchemistry.chemical_elementHippocampusBiologyCalciumHippocampusCalcium in biologyRats Sprague-DawleyInternal medicinemedicineAnimalsCalcium SignalingOrganic ChemicalsCells CulturedCellular SenescenceNeuronsCalcium metabolismCalpainGeneral NeuroscienceNeurodegenerationGlutamate receptorCalpainHydrogen PeroxideOxidantsmedicine.diseaseRatsOxidative Stressmedicine.anatomical_structureEndocrinologynervous systemchemistryNerve Degenerationbiology.proteinCalciumNeuronNeuroscienceNeuroscience Letters
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Exposure to gp120 of HIV-1 induces an increased release of arachidonic acid in rat primary neuronal cell culture followed by NMDA receptor-mediated n…

1995

After incubation of highly enriched neurons from rat cerebral cortex with the HIV-1 coat protein gp120 for 18 h, cells showed fragmentation of DNA at internucleosomal linkers followed by NMDA receptor-mediated neurotoxicity. We report that in response to exposure to gp120 cells react with an increased release of arachidonic acid (AA) via activation of phospholipase A2. This process was not inhibited by NMDA receptor antagonists. To investigate the role of AA on the sensitivity of the NMDA receptor towards its agonist, low concentrations of NMDA were co-administered with AA. This condition enhanced the NMDA-mediated cytotoxicity. Administration of mepacrine reduced cytotoxicity caused by gp1…

Agonistmedicine.drug_classNeurotoxinsPharmacologyHIV Envelope Protein gp120Receptors N-Methyl-D-Aspartatechemistry.chemical_compoundPhospholipase A2medicineAnimalsFragmentation (cell biology)Rats WistarCytotoxicityCells CulturedNeuronsArachidonic AcidbiologyCell DeathGeneral NeuroscienceNeurotoxicitymedicine.diseaseRatsnervous systemchemistryCell cultureQuinacrinebiology.proteinHIV-1NMDA receptorArachidonic acidDNA DamageThe European journal of neuroscience
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Novel imine antioxidants at low nanomolar concentrations protect dopaminergic cells from oxidative neurotoxicity.

2009

Strong evidence indicates that oxidative stress may be causally involved in the pathogenesis of Parkinson's disease. We have employed human dopaminergic neuroblastoma cells and rat primary mesencephalic neurons to assess the protective potential of three novel bisarylimine antioxidants on dopaminergic cell death induced by complex I inhibition or glutathione depletion. We have found that exceptionally low concentrations (EC(50) values approximately 20 nM) of these compounds (iminostilbene, phenothiazine, and phenoxazine) exhibited strong protective effects against the toxicities of MPP(+), rotenone, and l-buthionine sulfoximine. Investigating intracellular glutathione levels, it was found t…

Antioxidantmedicine.medical_treatmentDopamineGlutathione reductaseNeurotoxinsBiologymedicine.disease_causeProtein oxidationBiochemistryAntioxidantsLipid peroxidationRats Sprague-DawleyCellular and Molecular Neurosciencechemistry.chemical_compoundCell Line TumormedicineAnimalsHumansCells CulturedMembrane Potential MitochondrialCell DeathDose-Response Relationship DrugNeurotoxicityParkinson DiseaseRotenoneGlutathionemedicine.diseaseGlutathioneMitochondriaRatsSubstantia NigraOxidative StressNeuroprotective AgentschemistryBiochemistryElectron Transport Chain Complex ProteinsCytoprotectionNerve DegenerationIminesOxidation-ReductionOxidative stressJournal of neurochemistry
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Aß(25-35) and its C-and/or N-blocked derivatives: copper driven structural features and neurotoxicity

2006

The toxic properties of beta-amyloid protein, Abeta(1-42), the major component of senile plaques in Alzheimer's disease, depend on nucleation-dependent oligomerization and aggregation. In addition, Abeta(1-42) toxicity is favored by the presence of trace metals, which affect the secondary structure of the peptide. A peptide comprising 11 residues within Abeta(1-42) [Abeta(25-35)] aggregates and retains the neurotoxic activity of Abeta(1-42). We have used both Abeta(25-35) and its C-amidated or N-acetylated/C-amidated derivatives to investigate the role of copper(II) in modulating the conformation and aggregation state as well as the neurotoxic properties of amyloid peptides. Electrospray io…

Circular dichroismSpectrometry Mass Electrospray IonizationAmyloidProtein Conformationb-amyloidNeurotoxinsPeptideMicroscopy Atomic ForceCellular and Molecular NeuroscienceProtein structuremental disordersmedicineAnimalsSenile plaqueschemistry.chemical_classificationCerebral CortexNeuronsAmyloid beta-PeptidesCircular DichroismCopper toxicityNeurotoxicityP3 peptideElectron Spin Resonance SpectroscopyAlzheimer's diseasemedicine.diseasePeptide Fragmentsnervous system diseasesRatschemistryBiochemistrycopperModels AnimalBiophysicsAlzheimer’s disease
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Old Weapons for New Wars: Bioactive Molecules From Cnidarian Internal Defense Systems

2016

The renewed interest in the study of genes of immunity in Cnidaria has led to additional information to the scenario of the first stages of immunity evolution revealing the cellular processes involved in symbiosis, in the regulation of homeostasis and in the fight against infections. The recent study with new molecular and functional approach on these organisms have therefore contributed with unexpected information on the knowledge of the stages of capturing activities and defense mechanisms strongly associated with toxin production. Cnidarians are diblastic aquatic animals with radial symmetry; they represent the ancestral state of Metazoa, they are the simplest multicellular organisms tha…

CnidariaImmune defenseMicrobial toxinsbiologyPhylumEcologyGeneral NeuroscienceBioactive moleculesNeurotoxinsDefence mechanismsbiology.organism_classificationCnidariaMulticellular organismCnidarian VenomsNeuropsychology and Physiological PsychologyAnti-Infective AgentsAntimicrobial peptide Cnidaria Cytolysins Immune defense Neurotoxin ToxinsImmunityEvolutionary biologyAnimalsHumansMolecular MedicinePeptidesSodium Channel Blockers
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Reduction of red-green discrimination by dopamine D1 receptor antagonists and retinal dopamine depletion

1996

AbstractReduction of wavelength discrimination ability in the 560–640 nm range, but not in the 404–540 nm range, has been demonstrated in goldfish after intravitreal injection of D1-dopamine receptor antagonists. Intravitreal injection of the dopaminergic neurotoxin 6-OH-dopamine severely reduced wavelength discrimination ability in the 540–661 nm range within 3 days. Discrimination ability could be reconstituted by the Dl-agonist SKF 38393. Animals recovered from injection of 6-OH-dopamine within 14–16 days. No change of wavelength discrimination was induced by 6-OH-dopamine in the 461–540 nm range. We conclude that under photopic conditions dopamine modulates retinal mechanisms involved i…

DopamineWavelength discriminationRetinaHydroxydopamineschemistry.chemical_compoundDiscrimination PsychologicalDopamine receptor D1OpticsDopamineGoldfishmedicineAnimalsNeurotoxinDopamine receptorsNeurotransmitterRetinabusiness.industryReceptors Dopamine D1DopaminergicRetinalSensory SystemsOphthalmologymedicine.anatomical_structurechemistryDopamine receptorDopamine AgonistsBiophysicssense organsbusinessColor Perceptionmedicine.drugVision Research
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Structural brain network fingerprints of focal dystonia

2019

Background: Focal dystonias are severe and disabling movement disorders of a still unclear origin. The structural brain networks associated with focal dystonia have not been well characterized. Here, we investigated structural brain network fingerprints in patients with blepharospasm (BSP) compared with those with hemifacial spasm (HFS), and healthy controls (HC). The patients were also examined following treatment with botulinum neurotoxin (BoNT). Methods: This study included matched groups of 13 BSP patients, 13 HFS patients, and 13 HC. We measured patients using structural-magnetic resonance imaging (MRI) at baseline and after one month BoNT treatment, at time points of maximal and minim…

Dystoniagraph theory610 Medical sciencesblepharospasm610 Medizinbotulinum neurotoxinlcsh:Neurology. Diseases of the nervous systemlcsh:RC346-429Original ResearchMRIstructural brain networks
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Individual and Combined Effect of Zearalenone Derivates and Beauvericin Mycotoxins on SH-SY5Y Cells

2020

Beauvericin (BEA) and zearalenone derivatives, &alpha

FusariumMTTElectrosprayTime FactorsHealth Toxicology and MutagenesisNeurotoxinslcsh:MedicineToxicologyMass spectrometryArticleSH-SY5Y cells03 medical and health scienceschemistry.chemical_compoundInhibitory Concentration 500404 agricultural biotechnologyCell Line TumorDepsipeptidesHumansMTT assayMycotoxinZearalenone030304 developmental biologyNeurons0303 health scienceszearalenone derivatesChromatographybiologyCell DeathDose-Response Relationship Druglcsh:RbeauvericinDrug Synergism04 agricultural and veterinary sciencesbiology.organism_classification040401 food scienceBeauvericinqTOF–MS/MSchemistryZeranolAntagonismToxins
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Altered functional connectivity in blepharospasm/orofacial dystonia

2017

Abstract Introduction Blepharospasm is characterized by involuntary eyelid spasms. It can be associated with perioral dystonia (Meige's syndrome or orofacial dystonia). We aimed at studying resting‐state functional brain connectivity in these patients and its potential modulation by therapeutic botulinum toxin injections. Methods We performed resting‐state functional MRI and a region of interest‐based analysis of functional connectivity in 13 patients with blepharospasm/Meige's syndrome in comparison to 13 healthy controls. Patients were studied before and 4 weeks after botulinum toxin treatment. Simultaneous facial electromyography was applied to control for involuntary facial movements. R…

Male0301 basic medicineCingulate cortexBotulinum ToxinsBlepharospasmNeurotoxinsBlepharospasmSomatosensory systemMeige's syndrome03 medical and health sciencesBehavioral Neuroscience0302 clinical medicineCortex (anatomy)medicineHumansOriginal ResearchAgedDystoniaBrain MappingElectromyographyPostcentral gyrusbusiness.industryfunctional connectivityBrainMeige's syndromeMiddle Agedmedicine.diseaseMagnetic Resonance ImagingBotulinum toxineye diseasesddc:DystoniaTreatment Outcome030104 developmental biologymedicine.anatomical_structureorofacial dystoniaDystonic DisordersFemaleresting‐state functional MRImedicine.symptombusinessNeuroscience030217 neurology & neurosurgerymedicine.drugBrain and Behavior
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