Search results for "death"

showing 10 items of 1744 documents

Beauvericin-induced cytotoxicity via ROS production and mitochondrial damage in Caco-2 cells.

2013

The cytotoxicity of beauvericin (BEA) on human colon adenocarcinoma (Caco-2) cells was studied as a function of time. Moreover, the oxidative damage and cell death endpoints were monitored after 24, 48 and 72 h. After BEA exposure, the IC₅₀ values ranged from 1.9 ± 0.7 to 20.6 ± 6.9 μM. A decrease in reduced glutathione (GSH; 31%) levels, as well as an increase in oxidized glutathione (GSSG, 20%) was observed. In the presence of BEA, reactive oxygen species (ROS) level was highly increased at an early stage with the highest production of 2.0-fold higher than the control that was observed at 120 min. BEA induced cell death by mitochondria-dependent apoptotic process with loss of the mitochon…

G2 PhaseProgrammed cell deathDNA damageCell SurvivalApoptosisBiologyToxicologymedicine.disease_causechemistry.chemical_compoundInhibitory Concentration 50NecrosisDepsipeptidesmedicineHumansIntestinal Mucosachemistry.chemical_classificationMembrane Potential MitochondrialReactive oxygen speciesIonophoresCell growthGeneral MedicineGlutathioneMycotoxinsMolecular biologyGlutathioneBeauvericinCell biologyMitochondriaKineticsOxidative StresschemistryApoptosisLipid PeroxidationCaco-2 CellsReactive Oxygen SpeciesOxidation-ReductionOxidative stressDNA DamageToxicology letters
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TTAS a New Stilbene Derivative that Induces Apoptosis in Leishmania Infantum

2012

Leishmania parasites are able to undergo apoptosis (programmed cell death), similarly to mammalian cells. Recently it was demonstrated in vitro the anti-leishmanial effect of some natural and synthetic stilbenoids including resveratrol and piceatannol. In this study we evaluated the Leishmanicidal activity of a pool of stilbene derivatives which had previously shown high apoptotic efficacy against neoplastic cells. All the compounds tested were capable to decrease the parasite viability in a dose-dependent manner. Trans-stilbenes proved to be markedly more effective than cis-isomers. This was different from that observed in tumor cells in which cis-stilbenes were more potent cytotoxic agent…

G2 PhaseProgrammed cell deathLeishmaniasiSettore MED/17 - Malattie InfettiveImmunologyAntiprotozoal AgentsTUBULINApoptosisResveratrolChromatography AffinityLethal Dose 50chemistry.chemical_compoundGranulocyte-Macrophage Progenitor CellsAnnexin A5Leishmania infantumCytotoxicityCells CulturedMembrane Potential MitochondrialPiceatannolDose-Response Relationship DrugbiologyGeneral MedicineFlow CytometryHematopoietic Stem Cellsbiology.organism_classificationLeishmaniaPROGRAMMED CELL DEATHIn vitroInfectious DiseaseschemistryBiochemistrySTILBENESAntimony Sodium GluconateApoptosisStilbeneElectrophoresis Polyacrylamide GelParasitologyLeishmania infantumCell DivisionLEISHMANIASIS
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Staurosporine-induced apoptosis in Chang liver cells is associated with down-regulation of Bcl-2 and Bcl-XL.

2004

A potent inhibitor of serine/threonine kinases, staurosporine exerts antiproliferative and apoptotic effects in many cancer cells, although the exact mechanism of its action is still unclear. This study examines the effects of staurosporine on Chang liver cells, an immortalized non-tumor cell line, in comparison with those caused in HuH-6 and HepG2 cells, two human hepatoma cell lines. Our results provide evidence that staurosporine promotes apoptosis in Chang liver cells as observed by flow cytometric analysis and acridine orange/ethidium bromide staining. The effect appeared already after 8 h of treatment and increased with treatment time and dose. After 48 h of exposure to 200 nM stauros…

G2 PhaseProgrammed cell deathTime FactorsCell SurvivalLiver cytologyBlotting Westernbcl-X ProteinDown-RegulationMitosisApoptosisBcl-xLAmino Acid Chloromethyl KetonesCell LineMembrane PotentialsEthidiumSettore BIO/10 - BiochimicaGeneticsmedicineHumansStaurosporineEnzyme InhibitorsBcl-2 family factors.CaspaseApoptosis staurosporineDose-Response Relationship DrugbiologyCaspase 3Cell CycleGeneral MedicineFlow CytometryStaurosporineMolecular biologyAcridine OrangeMitochondriaEnzyme ActivationLiverProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureCaspasesCancer cellbiology.proteinCell Divisionmedicine.drug
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Synthesis and antiproliferative activity of thiazolyl-bis-pyrrolo[2,3-b]pyridines and indolyl-thiazolyl-pyrrolo[2,3-c]pyridines, nortopsentin analogu…

2015

Two new series of nortopsentin analogues, in which the imidazole ring of the natural product was replaced by thiazole and indole units were both substituted by 7-azaindole moieties or one indole unit was replaced by a 6-azaindole portion, were efficiently synthesized. Compounds belonging to both series inhibited the growth of HCT-116 colorectal cancer cells at low micromolar concentrations, whereas they did not affect the viability of normal-like intestinal cells. A compound of the former series induced apoptosis, evident as externalization of plasma membrane phosphatidylserine (PS), and changes of mitochondrial trans-membrane potential, while blocking the cell cycle in G2/M phase. In contr…

G2 Phaseantiproliferative activitybis-indolyl alkaloidsStereochemistryPyridinesPharmaceutical ScienceNortopsentin analoguesthiazolyl-bis-pyrrolo [23-b]pyridinesVacuoleArticlechemistry.chemical_compoundDrug DiscoveryImidazoleHumansPyrrolesautophagic deathThiazolelcsh:QH301-705.5Pharmacology Toxicology and Pharmaceutics (miscellaneous)Cell ProliferationIndole testMembrane Potential MitochondrialnortopsentinsDose-Response Relationship DrugMolecular Structureindolyl-thiazolyl-pyrrolo[23-c]pyridinesthiazolyl-bis-pyrrolo[23-b]pyridinesapoptosisPhosphatidylserineCell cycleHCT116 CellsSettore CHIM/08 - Chimica Farmaceuticaindolyl-thiazolyl-pyrrolo[23-<i>c</i>]pyridinesThiazoleslcsh:Biology (General)chemistryCytoplasmApoptosismarine alkaloidsthiazolyl-bis-pyrrolo [23-<i>b</i>]pyridinesMarine drugs
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Glutathione peroxidase-1 in health and disease: from molecular mechanisms to therapeutic opportunities.

2011

Reactive oxygen species, such as superoxide and hydrogen peroxide, are generated in all cells by mitochondrial and enzymatic sources. Left unchecked, these reactive species can cause oxidative damage to DNA, proteins, and membrane lipids. Glutathione peroxidase-1 (GPx-1) is an intracellular antioxidant enzyme that enzymatically reduces hydrogen peroxide to water to limit its harmful effects. Certain reactive oxygen species, such as hydrogen peroxide, are also essential for growth factor-mediated signal transduction, mitochondrial function, and maintenance of normal thiol redox-balance. Thus, by limiting hydrogen peroxide accumulation, GPx-1 also modulates these processes. This review explor…

GPX1AntioxidantPhysiologyProtein Conformationmedicine.medical_treatmentClinical BiochemistryMolecular Sequence DataGene ExpressionBiologymedicine.disease_causeBiochemistryDiabetes mellitus geneticschemistry.chemical_compoundGlutathione Peroxidase GPX1Risk FactorsComprehensive Invited ReviewNeoplasmsmedicineDiabetes MellitusAnimalsHumansGenetic Predisposition to DiseaseAmino Acid SequenceEnzyme InhibitorsHydrogen peroxideMolecular BiologyGeneral Environmental Sciencechemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidasePolymorphism GeneticCell DeathSuperoxideCell BiologyGlutathioneSelenocysteineOxidative StresschemistryBiochemistryGene Expression RegulationCardiovascular DiseasesGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidation-ReductionOxidative stressAntioxidantsredox signaling
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Galectin-3 Impairment of MYCN-Dependent Apoptosis-Sensitive Phenotype Is Antagonized by Nutlin-3 in Neuroblastoma Cells

2012

MYCN amplification occurs in about 20-25% of human neuroblastomas and characterizes the majority of the high-risk cases, which display less than 50% prolonged survival rate despite intense multimodal treatment. Somehow paradoxically, MYCN also sensitizes neuroblastoma cells to apoptosis, understanding the molecular mechanisms of which might be relevant for the therapy of MYCN amplified neuroblastoma. We recently reported that the apoptosis-sensitive phenotype induced by MYCN is linked to stabilization of p53 and its proapoptotic kinase HIPK2. In MYCN primed neuroblastoma cells, further activation of both HIPK2 and p53 by Nutlin-3 leads to massive apoptosis in vitro and to tumor shrinkage an…

Galectin 3Cancer TreatmentGene Dosagelcsh:MedicineApoptosisProtein-Serine-Threonine KinaseBiochemistryPiperazineschemistry.chemical_compoundNeuroblastoma0302 clinical medicineMolecular Cell BiologyBasic Cancer ResearchSignaling in Cellular Processeslcsh:ScienceEnergy-Producing OrganellesApoptotic SignalingNuclear ProteinOncogene Proteins0303 health sciencesN-Myc Proto-Oncogene ProteinMultidisciplinaryCell DeathImidazolesOncogene ProteinNuclear ProteinsTransfectionNutlin3. Good healthGene Expression Regulation NeoplasticProtein TransportCell killingPhenotypeOncologyGalectin-3030220 oncology & carcinogenesisGene Knockdown TechniquesMedicineResearch ArticleSignal TransductionHumanBiologyBioenergeticsProtein Serine-Threonine KinasesN-Myc Proto-Oncogene ProteinModels Biological03 medical and health sciencesNeuroblastomaCell Line TumormedicineHumansBiologyImidazolePiperazineneoplasms030304 developmental biologylcsh:RGene AmplificationChemotherapy and Drug Treatmentmedicine.diseasechemistryCell cultureApoptosisPediatric OncologyCytoprotectionGene Knockdown TechniqueCancer researchlcsh:QTumor Suppressor Protein p53Carrier ProteinsCarrier ProteinDNA Damage
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ΔNp73β is oncogenic in hepatocellular carcinoma by blocking apoptosis signaling via death receptors and mitochondria

2010

p73 belongs to the p53 family of transcription factors known to regulate cell cycle and apoptosis. The Trp73 gene has two promoters that drive the expression of two major p73 isoform subfamilies: TA and ΔN. In general, TAp73 isoforms show proapoptotic activities, whereas members of the N-terminally truncated (ΔN) p73 subfamily that lack the transactivation domain show antiapoptotic functions. We found that upregulation of ΔNp73 in hepatocellular carcinoma (HCC) correlated with reduced survival. Here, we investigated the molecular mechanisms accounting for the oncogenic role of ΔNp73 in HCC.ΔNp73β can directly interfere with the transcriptional activation function of the TA (containing the t…

Gene isoformCarcinoma HepatocellularMolecular Sequence DataApoptosisBiologyModels BiologicalTransactivationDownregulation and upregulationCell Line TumorHumansProtein IsoformsMolecular BiologyTranscription factorGenes DominantOligonucleotide Array Sequence Analysisbcl-2-Associated X ProteinRegulation of gene expressionBase SequenceSettore BIO/11Gene Expression ProfilingTumor Suppressor ProteinsLiver NeoplasmsNuclear ProteinsTumor Protein p73PromoterReceptors Death DomainCell BiologyCell cyclePrognosisMitochondriaCell biologyDNA-Binding ProteinsEnzyme ActivationGene Expression Regulation NeoplasticDrug Resistance NeoplasmCaspasesCancer researchTumor Suppressor Protein p53Signal transductionPrecancerous ConditionsSignal TransductionDevelopmental BiologyCell Cycle
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Logistic Growth Described by Birth-Death and Diffusion Processes

2019

We consider the logistic growth model and analyze its relevant properties, such as the limits, the monotony, the concavity, the inflection point, the maximum specific growth rate, the lag time, and the threshold crossing time problem. We also perform a comparison with other growth models, such as the Gompertz, Korf, and modified Korf models. Moreover, we focus on some stochastic counterparts of the logistic model. First, we study a time-inhomogeneous linear birth-death process whose conditional mean satisfies an equation of the same form of the logistic one. We also find a sufficient and necessary condition in order to have a logistic mean even in the presence of an absorbing endpoint. Then…

General MathematicsGompertz functionLogistic regressionConditional expectation01 natural sciencestransition probabilities03 medical and health sciencesFano factorComputer Science (miscellaneous)Applied mathematicsItô equationLimit (mathematics)0101 mathematicsLogistic functionStratonovich equationEngineering (miscellaneous)first-passage-time problem030304 developmental biologyMathematicslogistic model0303 health scienceslcsh:MathematicsItô equation010102 general mathematicsdiffusion processeslogistic model; birth-death process; first-passage-time problem; transition probabilities; Fano factor; coefficient of variation; diffusion processes; Itô equation; Stratonovich equation; diffusion in a potentiallcsh:QA1-939Birth–death processcoefficient of variationDiffusion processbirth-death processInflection pointdiffusion in a potentialMathematics
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Applying Benford’s Law to Monitor Death Registration Data: A Management Tool for the COVID-19 Pandemic

2021

In Spain, the COVID-19 pandemic has impacted the various regions of the country differ7 ently. The availability of reliable and up-to-date information has proved to be fundamental for the 8 management of this health crisis. However, especially during the first wave of the pandemic (Feb9 ruary-August 2020), the disparity in the recording criteria and in the timing of providing these fig10 ures to the central government created controversy and confusion regarding the real dimension of 11 the pandemic. It is therefore necessary to have objective and homogeneous criteria at the national 12 level to guide health managers in the correct recording and evaluation of the magnitude of the pan13 demic…

General Mathematicsreliability dataEstadísticahealth management toolSalut públicaCOVID-19 deathsComputer Science (miscellaneous)COVID-19 deaths; Benford’s Law; health management tool; reliability data; auditing toolQA1-939auditing toolEngineering (miscellaneous)MathematicsBenford’s LawMathematics
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Non-hermitian operator modelling of basic cancer cell dynamics

2018

We propose a dynamical system of tumor cells proliferation based on operatorial methods. The approach we propose is quantum-like: we use ladder and number operators to describe healthy and tumor cells birth and death, and the evolution is ruled by a non-hermitian Hamiltonian which includes, in a non reversible way, the basic biological mechanisms we consider for the system. We show that this approach is rather efficient in describing some processes of the cells. We further add some medical treatment, described by adding a suitable term in the Hamiltonian, which controls and limits the growth of tumor cells, and we propose an optimal approach to stop, and reverse, this growth.

General Physics and Astronomylcsh:AstrophysicsTumor cells01 natural sciencesArticle010305 fluids & plasmassymbols.namesakeOperatorial models; Schrödinger dynamics; non Hermitian Hamiltonian; Tumoral proliferation modelSchrödinger dynamicParticle number operatorlcsh:QB460-4660103 physical scienceslcsh:Science010306 general physicsSettore MAT/07 - Fisica MatematicaMathematical physicsPhysicsMedical treatmentOperatorial modelOther Quantitative Biology (q-bio.OT)Non hermitian HamiltonianTumoral proliferation modelQuantitative Biology - Other Quantitative Biologylcsh:QC1-999Birth–death processFOS: Biological sciencesSchrödinger dynamicsCancer cellsymbolslcsh:QOperatorial modelsHamiltonian (quantum mechanics)lcsh:PhysicsSelf-adjoint operator
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