Search results for "DEATH"

showing 10 items of 1744 documents

A Twin Protection Effect? Explaining Twin Survival Advantages with a Two-Process Mortality Model

2016

Twin studies that focus on the correlation in age-at-death between twin pairs have yielded important insights into the heritability and role of genetic factors in determining lifespan, but less attention is paid to the biological and social role of zygosity itself in determining survival across the entire life course. Using data from the Danish Twin Registry and the Human Mortality Database, we show that monozygotic twins have greater cumulative survival proportions at nearly every age compared to dizygotic twins and the Danish general population. We examine this survival advantage by fitting these data with a two-process mortality model that partitions survivorship patterns into extrinsic …

0301 basic medicineDeath RatesDenmarkPopulationTwinslcsh:MedicineSocial SciencesBiologyResearch and Analysis MethodsGeographical LocationsDanish03 medical and health sciences0302 clinical medicinePopulation MetricsSociologySurvivorship curveGeneticsMedicine and Health SciencesEthnicitiesPublic and Occupational Health030212 general & internal medicinelcsh:ScienceeducationDemographyeducation.field_of_studySocial ResearchMultidisciplinaryPopulation BiologyMortality ratelcsh:RBiology and Life SciencesHuman GeneticsHeritabilityDanesTwin studyZygositylanguage.human_languageEurope030104 developmental biologyResearch DesignPeople and PlacesTwin StudieslanguageLife course approachlcsh:QPopulation GroupingsBehavioral and Social Aspects of HealthResearch ArticleDemographyPLOS ONE
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A Multi-Parametric Fluorescent Assay for the Screening and Mechanistic Study of Drug-Induced Steatosis in Liver Cells in Culture.

2017

Human hepatic cells have been used for drug safety risk evaluations throughout early development phases. They provide rapid, cost-effective early feedback to identify drug candidates with potential hepatotoxicity. This unit presents a cell-based assay to evaluate the risk of liver damage associated with steatogenic drugs. Detailed protocols for cell exposure to test compounds and for the assessment of steatosis-related cell parameters (intracellular lipid content, reactive oxygen species production, mitochondrial impairment, and cell death) are provided. A few representative results that illustrate the utility of this procedure for the screening of drug-induced steatosis are shown. © 2017 b…

0301 basic medicineDrugProgrammed cell deathmedia_common.quotation_subjectCellMitochondria LiverBiologyToxicology03 medical and health sciencesmedicineHumansCells Culturedmedia_commonchemistry.chemical_classificationReactive oxygen speciesCell Deathmedicine.diseaseLipid MetabolismFatty Liver030104 developmental biologymedicine.anatomical_structurechemistryBiochemistryLiverHigh-content screeningCancer researchHepatic stellate cellHepatocytesSteatosisChemical and Drug Induced Liver InjuryReactive Oxygen SpeciesIntracellularCurrent protocols in toxicologyLiterature Cited
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Coexposure to sulfamethoxazole and cadmium impairs development and attenuates transcriptional response in sea urchin embryo

2017

Abstract Among sulfonamides, sulfamethoxazole represents one of the most widely employed. A considerable amount of sulfamethoxazole is introduced into the marine environment after utilization in aquaculture. The cytotoxicity of sulfamethoxazole relies mainly on arylhydroxylamine metabolites and it is associated with the production of reactive oxygen species. Cadmium represents a metal largely employed in several anthropic activities and it is toxic for all living organisms even at low concentrations. Since it is not degraded, cadmium irreversibly accumulates into cells. In order to understand the mechanisms of response to changes in the chemical environment, we investigated by light microsc…

0301 basic medicineEmbryo NonmammalianSulfamethoxazoleHealth Toxicology and Mutagenesis; Defense mechanisms;Gene ExpressionAquaculture010501 environmental sciencesmedicine.disease_cause01 natural sciencesCoexposureToxicologychemistry.chemical_compoundCadmium ChlorideGene expression profile; Stress responsechemistry.chemical_classificationCadmiumeducation.field_of_studyEchinodermSulfamethoxazoleChemistry (all)General MedicinePollutionCadmiumDefense mechanismEchinodermsmedicine.drugProgrammed cell deathEnvironmental EngineeringPopulationchemistry.chemical_elementSettore BIO/11 - Biologia MolecolareCadmium chlorideBiologyMicrobiologyCoexposure; Defense mechanisms; Echinoderms; Gene expression profile; Stress response; Chemistry (all); Environmental Chemistry03 medical and health sciencesDetoxificationmedicineAnimalsEnvironmental Chemistryeducation0105 earth and related environmental sciencesReactive oxygen speciesStress responsePublic Health Environmental and Occupational HealthGeneral ChemistryGene expression profile030104 developmental biologychemistrySea UrchinsWater Pollutants ChemicalOxidative stress
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Apoptosis induced by a HIPK2 full-length-specific siRNA is due to off-target effects rather than prevalence of HIPK2-Δe8 isoform

2017

Small interfering RNAs (siRNAs) are widely used to study gene function and extensively exploited for their potential therapeutic applications. HIPK2 is an evolutionary conserved kinase that binds and phosphorylates several proteins directly or indirectly related to apoptosis. Recently, an alternatively spliced isoform skipping 81 nucleotides of exon 8 (Hipk2-Δe8) has been described. Selective depletion of Hipk2 full-length (Hipk2-FL) with a specific siRNA that spares the Hipk2-Δe8 isoform has been shown to strongly induce apoptosis, suggesting an unpredicted dominant-negative effect of Hipk2-FL over the Δe8 isoform. From this observation, we sought to take advantage and assessed the therape…

0301 basic medicineGene isoformMaleProgrammed cell deathSmall interfering RNACell SurvivalBlotting WesternMice Nudecolorectal cancerApoptosisHIPK2BiologyProtein Serine-Threonine KinasesGene Expression Regulation Enzymologic03 medical and health sciencesExonRNA interferenceCell Line TumorAnimalsHumansViability assayoff-target effectCell Line TransformedSettore MED/04 - Patologia GeneraleKinaseReverse Transcriptase Polymerase Chain ReactionAlternative splicingalternative splicing isoformoff-target effectsExonsHCT116 CellsMolecular biologyXenograft Model Antitumor AssaysCell biologyGene Expression Regulation NeoplasticIsoenzymesAlternative Splicing030104 developmental biologyRNAi TherapeuticsOncologyalternative splicing isoformsNeoplastic Stem CellsRNA InterferenceHIPK2; alternative splicing isoforms; colorectal cancer; off-target effects; siRNA therapeutic applicationsiRNA therapeutic applicationCarrier ProteinsColorectal NeoplasmsGene DeletionResearch Paper
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Production Conditions Affect the In Vitro Anti-Tumoral Effects of a High Concentration Multi-Strain Probiotic Preparation.

2016

A careful selection of the probiotic agent, standardization of the dose and detailed characterization of the beneficial effects are essential when considering use of a probiotic for the dietary management of serious diseases. However, changes in the manufacturing processes, equipment or facilities can result in differences in the product itself due to the live nature of probiotics. The need to reconfirm safety and/or efficacy for any probiotic product made at a different factory is therefore mandatory. Recently, under the brand VSL#3®, a formulation produced by a manufacturer different from the previous one, has been commercialized in some European countries (the UK and Holland). VSL#3 is a…

0301 basic medicineGenetics and Molecular Biology (all)Cell LinesCancer Treatmentlcsh:MedicineApoptosisMedicine (all); Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)Biochemistrylaw.inventionProbiotic0302 clinical medicinelawMedicine and Health SciencesMedicineCell Cycle and Cell DivisionEnzyme-Linked Immunoassayslcsh:ScienceStainingMultidisciplinaryCell DeathMedicine (all)Inflammatory Bowel DiseasesCell StainingApoptotic deathProbiotic agentOncologyCell Processes030211 gastroenterology & hepatologyBiological CulturesResearch ArticleTumor cellsAffect (psychology)Research and Analysis MethodsMicrobiology03 medical and health sciencesImmunoassaysBeneficial effectsBacteriabusiness.industryProbioticslcsh:ROrganismsBiology and Life SciencesCell BiologyIn vitroBiotechnology030104 developmental biologyAgricultural and Biological Sciences (all)Specimen Preparation and TreatmentImmunologyImmunologic Techniqueslcsh:QCaco-2 CellsbusinessPLoS ONE
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Identification and Successful Negotiation of a Metabolic Checkpoint in Direct Neuronal Reprogramming

2016

Despite the widespread interest in direct neuronal reprogramming, the mechanisms underpinning fate conversion remain largely unknown. Our study revealed a critical time point after which cells either successfully convert into neurons or succumb to cell death. Co-transduction with Bcl-2 greatly improved negotiation of this critical point by faster neuronal differentiation. Surprisingly, mutants with reduced or no affinity for Bax demonstrated that Bcl-2 exerts this effect by an apoptosis-independent mechanism. Consistent with a caspase-independent role, ferroptosis inhibitors potently increased neuronal reprogramming by inhibiting lipid peroxidation occurring during fate conversion. Genome-w…

0301 basic medicineGeneticsProgrammed cell deathCell typeCellular Reprogramming TechniquesMutantCell BiologyBiologyIn vitroCell biology03 medical and health sciencesTransduction (genetics)030104 developmental biologyIn vivoGeneticsMolecular MedicineReprogrammingCell Stem Cell
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A dual role of caspase-8 in triggering and sensing proliferation-associated DNA damage, a key determinant of liver cancer development.

2017

Summary Concomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apop…

0301 basic medicineGenome instabilityMaleliver; Hepatocellular carcinoma; DNA damage response; replication stress; apoptosisCancer ResearchDNA RepairCarcinogenesisFas-Associated Death Domain ProteinApoptosisurologic and male genital diseasesDNA damage responseDna Damage Response ; Apoptosis ; Hepatocellular Carcinoma ; Liver ; Replication StressHistonesMice0302 clinical medicineRisk FactorsFADDPhosphorylationCellular SenescenceCaspase 8biologyLiver Neoplasmshepatocellular carcinomaLiver regeneration3. Good healthHistoneOncologyReceptors Tumor Necrosis Factor Type I030220 oncology & carcinogenesisReceptor-Interacting Protein Serine-Threonine KinasesFemalebiological phenomena cell phenomena and immunityCell agingCarcinoma HepatocellularDNA damageDNA repairreplication stressCaspase 8liverArticleGenomic Instability03 medical and health sciencesAnimalsHepatectomyHumansCrosses GeneticCell ProliferationJNK Mitogen-Activated Protein KinasesCell BiologyLiver Regeneration030104 developmental biologyImmunologyChronic Diseasebiology.proteinCancer researchHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinDNA Damage
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Evolutionary impact of copy number variation rates.

2017

[Objective]: Copy number variation is now recognized as one of the major sources of genetic variation among individuals in natural populations of any species. However, the relevance of these unexpected observations goes beyond diagnosing high diversity. [Results]: Here, it is argued that the molecular rates of copy number variation, mainly the deletion rate upon variation, determine the evolutionary road of the genome regarding size. Genetic drift will govern this process only if the efective population size is lower than the inverse of the deletion rate. Otherwise, natural selection will do.

0301 basic medicineGenome sizeDNA Copy Number VariationsGene duplicationPopulation geneticsPopulation geneticslcsh:MedicineBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesEffective population sizeGenetic driftGenetic variationAnimalsHumansCopy-number variationlcsh:Science (General)Genome sizelcsh:QH301-705.5GeneticsNatural selectionlcsh:RGenetic DriftBirth–death processGeneral MedicineBiological EvolutionResearch Note030104 developmental biologyGenetics Populationlcsh:Biology (General)Evolutionary biologyNeutral theory of molecular evolutionNeutral evolutionlcsh:Q1-390BMC research notes
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In vivo and in vitro effects of multiple sclerosis immunomodulatory therapeutics on glutamatergic excitotoxicity.

2015

In multiple sclerosis (MS), a candidate downstream mechanism for neuronal injury is glutamate (Glu)-induced excitotoxicity, leading to toxic increases in intraneuronal Ca(2+) . Here, we used in vivo two-photon imaging in the brain of TN-XXL transgenic Ca(2+) reporter mice to test whether promising oral MS therapeutics, namely fingolimod, dimethyl fumarate, and their respective metabolites fingolimod-phosphate and monomethyl fumarate, can protect neurons against acute glutamatergic excitotoxic damage. We also assessed whether these drugs can protect against excitotoxicity in vitro using primary cortical neurons, and whether they can directly inhibit Glu release from pathogenic T-helper 17 ly…

0301 basic medicineKainic acidMultiple SclerosisExcitotoxicityGlutamic AcidPharmacologyBiologymedicine.disease_causeBiochemistryNeuroprotectionImmunomodulation03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineIn vivomedicineAnimalsCells CulturedNeuronsKainic AcidDimethyl fumarateCell DeathGlutamate receptorNeurotoxicityBrainmedicine.diseaseUp-Regulation030104 developmental biologyNeuroprotective AgentschemistryNMDA receptor030217 neurology & neurosurgerySignal TransductionJournal of neurochemistry
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Phenolic extract from oleaster (Olea europaea var. Sylvestris) leaves reduces colon cancer growth and induces caspase-dependent apoptosis in colon ca…

2017

Erratum inCorrection: Phenolic extract from oleaster (Olea europaea var. Sylvestris) leaves reduces colon cancer growth and induces caspase-dependent apoptosis in colon cancer cells via the mitochondrial apoptotic pathway. [PLoS One. 2017]; International audience; Dietary polyphenols, derived from natural products, have received a great interest for their chemopreventive properties against cancer. In this study, we investigated the effects of phenolic extract of the oleaster leaves (PEOL) on tumor growth in mouse model and on cell death in colon cancer cell lines. We assessed the effect of oleaster leaf infusion on HCT116 (human colon cancer cell line) xenograft growth in athymic nude mice.…

0301 basic medicineLeavesCarcinoma Cellslcsh:MedicineApoptosisPlant ScienceMitochondrionEndoplasmic ReticulumBiochemistry[ SDV.CAN ] Life Sciences [q-bio]/Cancer0302 clinical medicineMedicine and Health SciencesMitochondrial calcium uptakeDiseaselcsh:ScienceEnergy-Producing OrganellesStainingchemistry.chemical_classificationSecretory PathwayMultidisciplinaryCell DeathPlant AnatomyCytochrome cCell StainingAnimal ModelsMitochondriaOlive Leaf ExtractChemistryOncologyExperimental Organism SystemsBiochemistryCell Processes030220 oncology & carcinogenesisPhysical SciencesCellular Structures and OrganellesResearch ArticleProgrammed cell deathActivationMouse Models[SDV.CAN]Life Sciences [q-bio]/CancerBioenergeticsBiologyResearch and Analysis MethodsColorectal-CancerCaspase-Dependent Apoptosis03 medical and health sciencesModel OrganismsPhenolsCytochrome-CColorectal CancerReactive oxygen speciesP53Cell growthProteinlcsh:RChemical CompoundsBiology and Life SciencesCancers and NeoplasmsPolyphenolsCell BiologyMolecular biology030104 developmental biologychemistrySpecimen Preparation and TreatmentApoptosisbiology.proteinCalciumlcsh:QPLoS ONE
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