Search results for "CASP"

showing 10 items of 470 documents

Distinct influence of atypical 1,4-dihydropyridine compounds in azidothymidine-induced neuro- and cardiotoxicity in mice ex vivo.

2008

This study demonstrates the effective protection by compounds of atypical 1,4-dihydropyridine (DHP) series cerebrocrast, glutapyrone and tauropyrone against neuro- and cardiotoxicity caused by the model compound azidothymidine, a well-known mitochondria-compromising anti-HIV drug. In previous in vitro experiments, we have demonstrated distinct effects of these DHP compounds to influence mitochondrial functioning. In the present in vivo experiments, DHP compounds were administered intraperitoneally in mice daily for 2 weeks, per se and in combinations with azidothymidine at doses: azidothymidine 50 mg/kg; cerebrocrast 0.1 mg/kg; glutapyrone 1 mg/kg; and tauropyrone 1 mg/kg. At the end of the…

MaleDihydropyridinesHeart DiseasesRatónAnti-HIV AgentsTaurineApoptosisBiologyPharmacologyToxicologyMiceGlutamatesIn vivomedicineAnimalsPharmacologyCerebral CortexInflammationCardiotoxicityMice Inbred ICRCaspase 3DihydropyridineTranscription Factor RelAGeneral MedicineBiochemistryGene Expression RegulationEnzyme inhibitorApoptosisToxicitybiology.proteinNeurotoxicity SyndromesZidovudineEx vivomedicine.drugBasicclinical pharmacologytoxicology
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Defective nuclear localization of Hsp70 is associated with dyserythropoiesis and GATA-1 cleavage in myelodysplastic syndromes.

2012

Abstract Normal human erythroid cell maturation requests the transcription factor GATA-1 and a transient activation of caspase-3, with GATA-1 being protected from caspase-3–mediated cleavage by interaction with the chaperone heat shock protein 70 (Hsp70) in the nucleus. Erythroid cell dysplasia observed in early myelodysplastic syndromes (MDS) involves impairment of differentiation and excess of apoptosis with a burst of caspase activation. Analysis of gene expression in MDS erythroblasts obtained by ex vivo cultures demonstrates the down-regulation of a set of GATA-1 transcriptional target genes, including GYPA that encodes glycophorin A (GPA), and the up-regulation of members of the HSP70…

MaleErythroblasts[SDV]Life Sciences [q-bio]Biochemistry0302 clinical medicineTranscription (biology)hemic and lymphatic diseasesGene expressionErythropoiesisGATA1 Transcription FactorCells CulturedCaspaseComputingMilieux_MISCELLANEOUSOligonucleotide Array Sequence AnalysisAged 80 and over0303 health sciencesbiologyCaspase 3Reverse Transcriptase Polymerase Chain ReactionCell DifferentiationU937 CellsHematologyMiddle Agedmedicine.anatomical_structure030220 oncology & carcinogenesisFemaleAdultGreen Fluorescent ProteinsImmunoblottingImmunology03 medical and health sciencesErythroid CellsmedicineHumansHSP70 Heat-Shock ProteinsTranscription factorAged030304 developmental biologyCell NucleusGene Expression ProfilingCell BiologyMolecular biologyCell nucleusMicroscopy FluorescenceApoptosisMyelodysplastic SyndromesChaperone (protein)Mutationbiology.proteinNuclear localization sequence
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IL-4 protects tumor cells from anti-CD95 and chemotherapeutic agents via up-regulation of antiapoptotic proteins

2004

Abstract We recently proposed that Th1 and Th2 cytokines exert opposite effects on the pathogenesis and clinical outcome of organ-specific autoimmunity by altering the expression of genes involved in target cell survival. Because a Th2 response against tumors is associated with poor prognosis, we investigated the ability of IL-4 to protect tumor cells from death receptor- and chemotherapy-induced apoptosis. We found that IL-4 treatment significantly reduced CD95 (Fas/APO-1)- and chemotherapeutic drug-induced apoptosis in prostate, breast, and bladder tumor cell lines. Analysis of antiapoptotic protein expression revealed that IL-4 stimulation resulted in up-regulation of cellular (c) FLIP/F…

MaleINFILTRATING LYMPHOCYTESCell SurvivalImmunologyCASP8 and FADD-Like Apoptosis Regulating Proteinbcl-X ProteinAntineoplastic AgentsApoptosisBreast NeoplasmsCARCINOMA-CELLSBiologySIGNALING PATHWAYSDownregulation and upregulationCell Line TumorImmunology and AllergyHumansfas ReceptorNON-HODGKINS-LYMPHOMACANCER PATIENTSReceptorBCL-2 PROTEINInterleukin 4EtoposideIL-4 apoptosis cancer stem cellsSettore MED/04 - Patologia GeneraleCHRONIC LYMPHOCYTIC-LEUKEMIAIntracellular Signaling Peptides and ProteinsAntibodies MonoclonalProstatic NeoplasmsFas receptorRecombinant ProteinsCell biologyUp-RegulationProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureFlipCancer researchT-CELLSCamptothecinFemaleInterleukin-4FLICE-INHIBITORY PROTEINSignal transductionCarrier ProteinsRENAL-CELL
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In vitro anticholinergic drugs affect CD8+ peripheral blood T-cells apoptosis in COPD

2011

Novel pharmacological strategies are aimed at the resolution of systemic inflammation in COPD potentiating peripheral blood T-cell (PBT-cell) apoptosis. Although muscarinic acetylcholine receptors (mAChRs) M(3) and choline-acetyltransferase (ChAT) participate in the airway inflammation of COPD, their role in PBT-cell apoptosis remains unexplained. We evaluated in PBT-cells from COPD patients, smoker (S) and control (C) subjects: (1) apoptosis (by annexin V binding), (2) mAChR M(3) and ChAT expression, acetylcholine (ACh)-binding; (3) choline levels in serum and PBT-cells extracts. We tested the effects of Tiotropium (Spiriva(®)) and hemicholinium-3 (HCh-3) on apoptosis, NFκB pathway, caspas…

MaleImmunologyScopolamine DerivativesApoptosisCD8-Positive T-LymphocytesPharmacologySystemic inflammationCholinergic AntagonistsCholineCholine O-AcetyltransferasePulmonary Disease Chronic ObstructiveAnnexinMuscarinic acetylcholine receptormedicineHumansImmunology and AllergyLymphocyte CountTiotropium BromideCaspaseAgedReceptor Muscarinic M3Caspase 8COPDbiologyCaspase 3Systemic inflammation Non-neuronal components of cholinergic system Caspases NF B pathwaybusiness.industryNF-kappa BHematologyTiotropium bromideMiddle Agedmedicine.diseaserespiratory tract diseasesEnzyme ActivationApoptosisbiology.proteinFemalemedicine.symptombusinessAcetylcholineProtein BindingSignal Transductionmedicine.drugImmunobiology
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Bruce/apollon promotes hippocampal neuron survival and is downregulated by kainic acid

2005

Prolonged or excess stimulation of excitatory amino acid receptors leads to seizures and the induction of excitotoxic nerve cell injury. Kainic acid acting on glutamate receptors produces degeneration of vulnerable neurons in parts of the hippocampus and amygdala, but the exact mechanisms are not fully understood. We have here investigated whether the anti-apoptotic protein Bruce is involved in kainic acid-induced neurodegeneration. In the rat hippocampus and cortex, Bruce was exclusively expressed by neurons. The levels of Bruce were rapidly downregulated by kainic acid in hippocampal neurons as shown both in vivo and in cell culture. Caspase-3 was activated in neurons exhibiting low level…

MaleKainic acidCell SurvivalBiophysicsExcitotoxicityBruce/apollon Hippocampus Kainic acid Excitotoxicity Neuronal death Caspase-3 Cytochrome cDown-RegulationHippocampusStimulationBiologyHippocampal formationmedicine.disease_causeHippocampusBiochemistrychemistry.chemical_compoundDownregulation and upregulationmedicineAnimalsRats WistarMolecular BiologyCells CulturedNeuronsKainic AcidDose-Response Relationship DrugNeurodegenerationGlutamate receptorCell Biologymedicine.diseaseRatsCell biologynervous systemchemistryBiochemistryUbiquitin-Conjugating Enzymeshuman activitiescirculatory and respiratory physiology
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MALT1 is deregulated by both chromosomal translocation and amplification in B-cell non-Hodgkin lymphoma

2003

The MALT1 gene was identified through its involvement in t(11;18)(q21;q21), seen in 30% of cases of mucosa-associated lymphoid tissue (MALT) lymphoma. Here, we show that deregulated MALT1 expression may occur in B-cell non-Hodgkin lymphoma (B-NHL) of various histologic subtypes either through translocation to the immunoglobulin heavy chain (IGH) locus or by genomic amplification. First, 2 cases, one case of MALT lymphoma and another of aggressive marginal zone lymphoma (MZL) with t(14;18)(q32;q21), cytogenetically identical to the translocation involving BCL2, were shown by fluorescence in situ hybridization (FISH) to involve MALT1, which lies about 5 Mb centromeric of BCL2. Molecular cloni…

MaleLymphoma B-CellImmunologyBiologyBiochemistryTranslocation Geneticimmune system diseaseshemic and lymphatic diseasesGene duplicationmedicineHumansRNA NeoplasmAgedChromosomes Human Pair 14medicine.diagnostic_testGene Expression ProfilingGene AmplificationMALT lymphomaLymphoma B-Cell Marginal ZoneCell BiologyHematologyMiddle Agedmedicine.diseaseMolecular biologyGenes bcl-2Neoplasm ProteinsGene Expression Regulation NeoplasticGene expression profilingMALT1Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinCaspasesB-Cell Non-Hodgkin LymphomaImmunoglobulin heavy chainFemaleChromosomes Human Pair 18Comparative genomic hybridizationFluorescence in situ hybridizationBlood
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The Long-Term Effect of Sevoflurane on Neuronal Cell Damage and Expression of Apoptotic Factors After Cerebral Ischemia and Reperfusion in Rats

2006

We investigated the long-term effects of sevoflurane on histopathologic injury and key proteins of apoptosis in a rat hemispheric ischemia/reperfusion model. Sixty-four male Sprague-Dawley rats were randomly assigned to Group 1 (fentanyl and N2O/O2; control) and Group 2 (2.0 vol% sevoflurane and O2/air). Ischemia (45 min) was produced by unilateral common carotid artery occlusion plus hemorrhagic hypotension (mean arterial blood pressure 40 mm Hg). Animals were killed after 1, 3, 7, and 28 days. In hematoxylin and eosin-stained brain sections eosinophilic hippocampal neurons were counted. Activated caspase-3 and the apoptosis-regulating proteins Bax, Bcl-2, Mdm-2, and p53 were analyzed by i…

MaleMethyl Ethersmedicine.medical_specialtyH&E stainIschemiaCell CountHippocampal formationHippocampusNeuroprotectionSevofluraneBrain IschemiaRats Sprague-DawleySevofluraneInternal medicineEosinophilicmedicineAnimalsNeuronsCaspase 3business.industrymedicine.diseaseImmunohistochemistryRatsEnzyme ActivationNeuroprotective AgentsAnesthesiology and Pain MedicineBlood pressureEndocrinologyCaspasesCerebrovascular CirculationReperfusion InjuryAnesthesiaAnesthetics InhalationApoptosis Regulatory ProteinsbusinessBlood Flow VelocityImmunostainingmedicine.drugAnesthesia & Analgesia
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Mitochondrial biogenesis fails in secondary biliary cirrhosis in rats leading to mitochondrial DNA depletion and deletions

2011

Chronic cholestasis is characterizedby mitochondrial dysfunction, associated with loss of mitochondrialmembrane potential, decreased activities of respiratory chaincomplexes, and ATP production. Our aim was to determine themolecular mechanisms that link long-term cholestasis to mitochondrialdysfunction. We studied a model of chronic cholestasis inducedby bile duct ligation in rats. Key sensors and regulators of theenergetic state and mitochondrial biogenesis, mitochondrial DNA(mtDNA)-to-nuclear DNA (nDNA) ratio (mtDNA/nDNA) relativecopy number, mtDNA deletions, and indexes of apoptosis (BAX,BCL-2, and cleaved caspase 3) and cell proliferation (PCNA) wereevaluated. Our results show that long…

MaleMitochondrial DNAPhysiologyMitochondrial TurnoverMitochondrial HepatopathyNF-E2-Related Factor 1Respiratory chainMitochondria LiverProtein Serine-Threonine KinasesMitochondrionBiologyDNA MitochondrialSirtuin 1CholestasisProliferating Cell Nuclear AntigenPhysiology (medical)medicineAnimalsRats Wistarbcl-2-Associated X ProteinCholestasisHepatologyCaspase 3Liver Cirrhosis BiliaryGastroenterologyPyruvate Dehydrogenase Acetyl-Transferring KinaseRNA-Binding ProteinsTFAMmedicine.diseaseGA-Binding Protein Transcription FactorPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMolecular biologyRatsGenes MitochondrialProto-Oncogene Proteins c-bcl-2Mitochondrial biogenesisChronic DiseaseBile DuctsGene DeletionTranscription FactorsAmerican Journal of Physiology-Gastrointestinal and Liver Physiology
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Controlled reperfusion after hypothermic heart preservation inhibits mitochondrial permeability transition-pore opening and enhances functional recov…

2006

We investigated whether low-pressure reperfusion may attenuate postischemic contractile dysfunction, limits necrosis and apoptosis after a prolonged hypothermic ischemia, and inhibits mitochondrial permeability transition-pore (MPTP) opening. Isolated rats hearts ( n = 72) were exposed to 8 h of cold ischemia and assigned to the following groups: 1) reperfusion with low pressure (LP = 70 cmH2O) and 2) reperfusion with normal pressure (NP = 100 cmH2O). Cardiac function was assessed during reperfusion using the Langendorff model. Mitochondria were isolated, and the Ca2+resistance capacity (CRC) of the MPTP was determined. Malondialdehyde (MDA) production, caspase-3 activity, and cytochrome c …

MaleNecrosisPhysiologyIschemiaHeart preservationMyocardial IschemiaMyocardial ReperfusionPharmacologyBiologyMitochondrionMitochondrial Membrane Transport ProteinsMitochondria HeartPermeabilityHypothermia InducedPhysiology (medical)MalondialdehydemedicinePressureAnimalsRats WistarCaspase 3Mitochondrial Permeability Transition PoreMyocardiumCytochromes cRecovery of Functionmedicine.diseaseFunctional recoveryRatsMitochondrial permeability transition poreApoptosisAnesthesiaCalciummedicine.symptomCardiology and Cardiovascular MedicineAmerican journal of physiology. Heart and circulatory physiology
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A possible biomarker for methadone related deaths

2017

Abstract Methadone (MTH) concentrations in those dying of MTH toxicity totally overlap concentrations where the presence of MTH is only an incidental finding, making it very difficult to make distinctions in actual cases. A biomarker, be it anatomical or biochemical for MTH toxicity is badly needed, particularly if that markers were known to disrupt effective ventilation. Because the brainstem houses the regulatory centers for cardiorespiratory-control enters, it would seem to be the most likely anatomical site to seek abnormalities in cardiorespiratory control. Objective To locate and describe the cells of nucleus of the solitary tract (TS)(NTS) in human brainstem and determine if neuronal…

MalePathologyNecrosisApoptosisAutopsyCohort Studies0302 clinical medicineRetrospective StudieMedicineForensic PathologyNeuronsPoisoningSolitary tractGeneral MedicineRostral ventrolateral medullaNecrosiImmunohistochemistryCaspase 9Narcotic030220 oncology & carcinogenesisToxicityFemaleBrainstemmedicine.symptomBrainstemCaspase-9HumanNarcoticsAdultProgrammed cell deathmedicine.medical_specialty2734Pathology and Forensic MedicineNecrosisForensic ToxicologyYoung Adult03 medical and health sciencesSettore MED/43 - Medicina LegaleSolitary NucleuSolitary NucleusNeurotoxicityHumansRetrospective Studiesbusiness.industryfungiApoptosiBiomarkerNeuronApoptosisApoptosis; Biomarker; Brainstem; Caspase-9; Methadone; Neurotoxicity; Adult; Apoptosis; Brain Stem; Caspase 9; Cohort Studies; Female; Forensic Pathology; Forensic Toxicology; Humans; Immunohistochemistry; Male; Methadone; Narcotics; Necrosis; Neurons; Poisoning; Retrospective Studies; Solitary Nucleus; Young Adult; 2734; LawCohort StudiebusinessLawMethadone030217 neurology & neurosurgeryBrain Stem
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