Search results for "Neurotoxicity"

showing 10 items of 105 documents

Triclosan-Evoked Neurotoxicity Involves NMDAR Subunits with the Specific Role of GluN2A in Caspase-3-Dependent Apoptosis

2018

Triclosan (TCS) is an antimicrobial agent that is used extensively in personal care and in sanitising products. A number of studies have shown the presence of TCS in different human tissues such as blood, adipose tissue, the liver, brain as well as in breast milk and urine. N-Methyl-D-aspartate receptors (NMDARs) are glutamate-gated ion channels that are widely expressed in the central nervous system and which play key roles in excitatory synaptic transmission. There is, however, no data on the involvement of NMDAR subunits in the apoptotic and neurotoxic effects of TCS. Our experiments are the first to show that TCS used at environmentally relevant concentrations evoked NMDA-dependent effe…

0301 basic medicineProgrammed cell deathGluN1Protein subunitNeurotoxinsNeuroscience (miscellaneous)Glutamic AcidCaspase 3ApoptosisReceptors N-Methyl-D-AspartateArticle03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicinemedicineAnimalsGene SilencingRNA MessengerReceptorNeuronsL-Lactate DehydrogenaseChemistryCaspase 3fungiNeurotoxicityROSTransfectionmedicine.diseaseTriclosanCell biologyGluN2BGluN2AProtein Subunits030104 developmental biologyNeurologyNMDAApoptosisNMDA receptorFemale030217 neurology & neurosurgeryMolecular Neurobiology
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Molecular chaperones in the brain endothelial barrier: neurotoxicity or neuroprotection?

2019

Brain microvascular endothelial cells (BMECs) interact with astrocytes and pericytes to form the blood-brain barrier (BBB). Their compromised function alters the BBB integrity, which is associated with early events in the pathogenesis of cancer, neurodegenerative diseases, and epilepsy. Interestingly, these conditions also induce the expression of heat shock proteins (HSPs). Here we review the contribution of major HSP families to BMEC and BBB function. Although investigators mainly report protective effects of HSPs in brain, contrasted results were obtained in BMEC, which depend both on the HSP and on its location, intra- or extracellular. The therapeutic potential of HSPs must be scrupulo…

0301 basic medicineReviewBiochemistryNeuroprotectionPathogenesis03 medical and health sciencesEpilepsy0302 clinical medicineHeat shock proteinGeneticsExtracellularMedicineAnimalsHumansMolecular Biologybusiness.industryNeurotoxicityCancerBrainEndothelial CellsBiological TransportCell Differentiationmedicine.diseaseNeuroprotectionCell biology030104 developmental biologyBlood-Brain Barriercardiovascular systembusiness030217 neurology & neurosurgeryFunction (biology)BiotechnologyMolecular ChaperonesFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Hippocampal hyperexcitability is modulated by microtubule-active agent: evidence from in vivo and in vitro epilepsy models in the rat

2016

The involvement of microtubule dynamics on bioelectric activity of neurons and neurotransmission represents a fascinating target of research in the context of neural excitability. It has been reported that alteration of microtubule cytoskeleton can lead to profound modifications of neural functioning, with a putative impact on hyperexcitability phenomena. Altogether, in the present study we pointed at exploring the outcomes of modulating the degree of microtubule polymerization in two electrophysiological epileptiform activity in the rat hippocampus. To this aim, we used in vivo Maximal Dentate Activation (MDA) and in vitro hippocampal epileptiform bursting activity (HEBA) paradigms to asse…

0301 basic medicinehippocampusPaclitaxel.HippocampusContext (language use)BiologyNeurotransmissionHippocampal formationSettore BIO/09 - Fisiologialcsh:RC321-571Microtubule polymerization03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compoundpaclitaxel0302 clinical medicineMicrotubulemedicinelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryOriginal ResearchNeurotoxicitymedicine.diseaseelectrophysiologyNocodazole030104 developmental biologynocodazolechemistryepilepsyhippocampus epilepsy maximal dentate activation microtubule electrophysiology nocodazole paclitaxel.maximal dentate activationNeuroscience030217 neurology & neurosurgeryNeurosciencemicrotubule
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Triclosan activates aryl hydrocarbon receptor (AhR)-dependent apoptosis and affects Cyp1a1 and Cyp1b1 expression in mouse neocortical neurons.

2016

Triclosan (TCS) is an antimicrobial agent that is used extensively in personal care and in sanitizing products, such as soaps, toothpastes, and hair products. A number of studies have revealed the presence of TCS in human tissues, such as fat, liver and brain, in addition to blood and breast milk. The aim of the present study was to investigate the impact of TCS on AhR and Cyp1a1/Cyp1b1 signaling in mouse neocortical neurons in primary cultures. In addition to the use of selective ligands and siRNAs, expression levels of mRNA and proteins as well as caspase-3 activity, reactive oxygen species (ROS) formation, and lactate dehydrogenase (LDH) release have been measured. We also studied the in…

0301 basic medicinemedicine.medical_specialtySmall interfering RNAStimulationCaspase 3ApoptosisNeocortex010501 environmental sciencesBiology01 natural sciencesBiochemistry03 medical and health sciencesMiceInternal medicinemedicineCytochrome P-450 CYP1A1Cyp1a1AnimalsRNA MessengerCells Cultured0105 earth and related environmental sciencesGeneral Environmental Sciencechemistry.chemical_classificationNeuronsReactive oxygen speciesCaspase 3fungiAhRNeurotoxicityCyp1b1respiratory systemNeuronmedicine.diseaseAryl hydrocarbon receptorTriclosanCell biology030104 developmental biologyEndocrinologyMechanism of actionchemistryReceptors Aryl HydrocarbonApoptosisCytochrome P-450 CYP1B1biology.proteinAnti-Infective Agents LocalFemalemedicine.symptomReactive Oxygen SpeciesEnvironmental research
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The hard road to data interpretation: 3 or 6 months of adjuvant chemotherapy for patients with stage III colon cancer?

2019

Background Six months of adjuvant oxaliplatin-based chemotherapy is standard for patients with stage III colon cancer following surgery. However, oxaliplatin is associated with peripheral neurotoxicity which worsens over treatment duration. Consequently, a shorter treatment duration, if equally effective, would be extremely beneficial. A pooled analysis of data for 12 834 stage III colon cancer patients, from six randomised phase III trials of adjuvant therapy, the International Duration Evaluation of Adjuvant chemotherapy study, was carried out and the results presented at the ASCO Annual Meeting 2017. To clarify the potential impact of these results on clinical practice, ESMO decided to s…

0301 basic medicinemedicine.medical_specialtyTime FactorsColorectal cancerRisk AssessmentDisease-Free Survival03 medical and health sciences0302 clinical medicineFOLFOXInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineAdjuvant therapyHumansMulticenter Studies as TopicColectomyNeoplasm StagingRandomized Controlled Trials as Topicbusiness.industryCAPOX RegimenHematologyCongresses as Topicmedicine.diseaseChemotherapy regimenOxaliplatinClinical trialOxaliplatinRegimen030104 developmental biologyOncologyClinical Trials Phase III as TopicChemotherapy Adjuvant030220 oncology & carcinogenesisData Interpretation StatisticalColonic NeoplasmsPractice Guidelines as TopicQuality of LifeNeurotoxicity Syndromesbusinessmedicine.drugAnnals of oncology : official journal of the European Society for Medical Oncology
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Increased frequency of proinflammatory CD4 T cells and pathological levels of serum neurofilament light chain in adult drug-resistant epilepsy

2020

OBJECTIVE: Adult drug-resistant epilepsy (DRE) is associated with significant morbidity. Infiltration of immune cells is observed in DRE epileptic foci; however, the relation between DRE and the peripheral immune cell compartment remains only partially understood. We aimed to investigate differences in immune cell populations, cytokines, and neurodegenerative biomarkers in the peripheral blood of subjects with epilepsy versus healthy controls, and in DRE compared to well-controlled epilepsy (WCE). METHODS: Peripheral blood mononuclear cells and serum from >120 age- and sex-matched adults suffering from focal onset epilepsy and controls were analyzed by multipanel flow cytometry, multiplex i…

AdultCD4-Positive T-LymphocytesMale0301 basic medicineDrug Resistant Epilepsymedicine.medical_treatmenturologic and male genital diseasesPeripheral blood mononuclear cellProinflammatory cytokineInterferon-gammaYoung Adult03 medical and health sciencesEpilepsyTh2 Cells0302 clinical medicineImmune systemNeurofilament ProteinsmedicineHumansImmunoassayInflammationEpilepsyTumor Necrosis Factor-alphabusiness.industryInterleukinsInterleukin-17NeurotoxicityGranulocyte-Macrophage Colony-Stimulating FactorInterleukinMiddle AgedFlow Cytometrymedicine.diseaseSingle Molecule ImagingCD4 Lymphocyte CountInterleukin-10030104 developmental biologyCytokineNeurologyCase-Control StudiesImmunologyCytokinesTh17 CellsFemaleTumor necrosis factor alphaInterleukin-4Neurology (clinical)business030217 neurology & neurosurgery
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Gemcitabine (GEM) plus oxaliplatin, folinic acid, and 5-fluorouracil (FOLFOX-4) in patients with advanced gastric cancer

2005

Abstract BACKGROUND AND AIMS: oxaliplatin in combination with folinic acid (FA) and infusional 5-fluorouracil (5-FU) has shown significant anti-tumor activity in gastric cancer patients (FOLFOX). Previous studies have shown that gemcitabine (GEM), a new fluorinated anti-metabolite, enhances the individual anti-tumor activity of either 5-FU or oxaliplatin. We have therefore designed a multi-center phase II trial in order to test a novel GEM+FOLFOX-4 regimen in patients with metastatic gastric cancer. METHODS: we enrolled 36 patients, 28 males and 8 females, with an average age of 64.4 years (range 37-78), who received bi-weekly treatment with GEM (1,000 mg/m2 on day 1), levo-FA (100 mg/m2 on…

AdultMaleAntimetabolites AntineoplasticCancer Researchmedicine.medical_specialtyOrganoplatinum CompoundsGastrointestinal Diseasesmedicine.drug_classfolinic acidmedicine.medical_treatmentLeucovorinAdenocarcinomaToxicologyDeoxycytidineAntimetaboliteGastroenterologyFolinic acidFOLFOXStomach NeoplasmsInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumans5-fluorouracilPharmacology (medical)Infusions IntravenousAgedNeoplasm StagingPharmacologyChemotherapybusiness.industrygastric canceroxaliplatingemcitabineMiddle AgedHematologic DiseasesGemcitabineSurgeryOxaliplatinSurvival RateRegimenOncologyFluorouracilFemaleNeurotoxicity SyndromesFluorouracilbusinessmedicine.drugCancer Chemotherapy and Pharmacology
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Pharmacological intervention in age-associated brain disorders by Flupirtine: Alzheimer’s and Prion diseases

1998

Alzheimer's disease, a major form of dementia in the elderly has become an increasingly important health problem in developed countries. In vitro studies on primary neurons demonstrate that Flupirtine (Katadolon) at a concentration of 1 microg/ml, significantly reduces the neurotoxic (apoptotic) effect displayed by A beta25-35, a segment of the amyloid beta-protein precursor the etiologic agent of Alzheimer's disease. Flupirtine, which has been in clinical use since 10 years ago, prevents the toxic effect of PrP, the presumed etiologic agent of the Creutzfeldt-Jakob disease as well as the excitatory amino acid glutamate on cortical neurons. Flupirtine displays a bimodal activity. Its strong…

AgingTime FactorsCell SurvivalPrionsMolecular Sequence DataAminopyridinesApoptosisPharmacologyBiologyNeuroprotectionPrion Diseaseschemistry.chemical_compoundGlutamatesAlzheimer DiseasemedicineAnimalsAmino Acid SequenceRats WistarCells CulturedNeuronsAmyloid beta-PeptidesGlutamate receptorNeurotoxicityBiological activityGlutathionemedicine.diseasePeptide FragmentsRatsNeuroprotective Agentsmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2BiochemistrychemistryCalciumNeuronAlzheimer's diseaseFlupirtineDevelopmental Biologymedicine.drugMechanisms of Ageing and Development
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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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Cellular Prion Protein Participates in Amyloid-β Transcytosis across the Blood—Brain Barrier

2012

The blood—brain barrier (BBB) facilitates amyloid-β (Aβ) exchange between the blood and the brain. Here, we found that the cellular prion protein (PrPc), a putative receptor implicated in mediating Aβ neurotoxicity in Alzheimer's disease (AD), participates in Aβ transcytosis across the BBB. Using an in vitro BBB model, [125I]-Aβ1–40 transcytosis was reduced by genetic knockout of PrPc or after addition of a competing PrPc-specific antibody. Furthermore, we provide evidence that PrPc is expressed in endothelial cells and, that monomeric Aβ1–40 binds to PrPc. These observations provide new mechanistic insights into the role of PrPc in AD.

Amyloid βanimal diseasesBiologyBrief CommunicationBlood–brain barrierModels BiologicalMiceAlzheimer Diseasemental disordersmedicineAnimalsPrPC ProteinsPrion proteinReceptorCells CulturedAmyloid beta-PeptidesNeurotoxicitymedicine.diseaseMolecular biologyPeptide FragmentsIn vitronervous system diseasesCell biologymedicine.anatomical_structureNeurologyTranscytosisBlood-Brain BarrierGene Knockdown Techniquesbiology.proteinNeurology (clinical)AntibodyTranscytosisCardiology and Cardiovascular MedicineProtein BindingJournal of Cerebral Blood Flow & Metabolism
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