Search results for "DAMAGE"

showing 10 items of 1289 documents

On the nuclear response of the helium-cooled lithium lead test blanket module in ITER

2005

Abstract The helium-cooled lithium lead (HCLL) concept has been recently selected as one of the two European reference designs foreseen for the breeding blanket of a demonstration fusion reactor. In particular, within the framework of the research and development activities on this blanket line, an HCLL test blanket module (TBM) has to be designed and manufactured to be implemented in ITER. At the Department of Nuclear Engineering (DIN) of the University of Palermo, a research campaign has been carried out to investigate the nuclear response of HCLL-TBM inside ITER by a numerical approach based on the Monte Carlo method. A realistic 3D heterogeneous model of HCLL-TBM has been set-up and ins…

CryostatMaterials scienceMechanical EngineeringNuclear engineeringMonte Carlo methodchemistry.chemical_elementBlanketFusion powerNuclear Energy and EngineeringchemistryTest blanket moduleHCLL-blanketNeutronicsRadiation damageNeutron sourceGeneral Materials ScienceLithiumSettore ING-IND/19 - Impianti NucleariHeliumCivil and Structural EngineeringFusion Engineering and Design
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Ab initio modeling of radiation damage in MgF2 crystals

2014

Abstract MgF2 with a rutile structure is important radiation-resistant material with numerous applications due to its transparency from vacuum ultraviolet to infrared range of photon energies. We present and discuss the results of calculations for basic radiation defects in this crystal. The study is based on the large scale ab initio DFT calculations using hybrid B3PW exchange–correlation functional and atomic basis set. We analyzed the electronic structure, atomic displacements, charge density distribution as well as defect formation energies using large supercells. We compared properties of close and well separated F−H (Frenkel) defect pairs as well as individual defects. We simulated al…

CrystalCondensed Matter::Materials ScienceNuclear and High Energy PhysicsPhotonInfraredChemistryAb initioRadiation damageCharge densityElectronic structureAtomic physicsInstrumentationBasis setNuclear Instruments and Methods in Physics Research Section B: Beam Interactions with Materials and Atoms
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Radiation damage in zircon

2003

A single, zoned, Sri Lankan zircon exhibits a range of microstructures from crystalline to nearly amorphous that are the result of radiation damage over a dose range of 2.1–10.1·1015 α-decay events/mg (0.16–0.47 dpa). The zones in the crystal were examined at a variety of length scales using optical microscopy, micro-Raman spectroscopy, electron microprobe analysis, and transmission electron microscopy. Birefringence varies linearly with dose: birefringence = −4.71·10−18 /g· D α + 4.86·10−2. Full width at half maximum (FWHM) measurements of the B1g(ν3) peak, as determined by micro-Raman spectroscopy, were used to estimate the extent of radiation damage in each zone. The radiation dose (calc…

CrystalFull width at half maximumGeophysicsGeochemistry and PetrologyTransmission electron microscopyAnalytical chemistryRadiation damageMineralogyElectron microprobeSpectroscopyGeologyZirconAmorphous solidAmerican Mineralogist
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<title>Heavy-ion induced damage and reduction of dislocation mobility in LiF single crystals</title>

2006

Ion-induced reduction of dislocation mobility in LiF crystals irradiated with swift heavy (U) and light (Ni) ions of a specific energy of 11 MeV per nucleon at fluences between 106 and 1011 ions/cm2 was studied. The arm length of dislocation rosettes produced by indentation on (100) irradiated surface was measured. It has been found that in the case of heavy ions the threshold fluence (106 ions/cm2) for impeding of dislocation arms is about 3 orders of magnitude lower than that for light ions. The results indicate that ion-induced defect aggregates play the dominating role in the impeding of dislocations. Heavy ions, which produce defect aggregates in the track core, cause also a stronger e…

CrystallographyMaterials sciencePhysics::Plasma PhysicsRadiation damageSurface modificationIrradiationOrders of magnitude (numbers)DislocationLaser-induced fluorescenceFluenceMolecular physicsIonSPIE Proceedings
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Miltirone Induces G2/M Cell Cycle Arrest and Apoptosis in CCRF-CEM Acute Lymphoblastic Leukemia Cells

2015

Miltirone (1) is a diterpene quinone extracted from a well-known Chinese traditional herb (Salvia miltiorrhiza). We investigated the cytotoxic effects of miltirone toward sensitive and multidrug-resistant acute lymphoblastic leukemia cell lines. Miltirone inhibited multidrug-resistant P-glycoprotein (P-gp)-overexpressing CEM/ADR5000 cells better than drug-sensitive CCRF-CEM wild-type cells, a phenomenon termed collateral sensitivity. Flow cytometric analyses revealed that miltirone induced G2/M arrest and apoptosis. Furthermore, miltirone stimulated reactive oxygen species (ROS) generation and mitochondrial membrane potential (MMP) disruption, which in turn induced DNA damage and activation…

Cyclin-Dependent Kinase Inhibitor p21ATP Binding Cassette Transporter Subfamily BDNA damagePoly ADP ribose polymeraseCellPharmaceutical ScienceApoptosisSalvia miltiorrhizaAnalytical ChemistryDrug DiscoverymedicineHumansCyclin B1CaspaseMembrane Potential MitochondrialPharmacologyCyclin-dependent kinase 1Molecular StructurebiologyOrganic ChemistryPhenanthrenesPrecursor Cell Lymphoblastic Leukemia-LymphomaMolecular biologyG2 Phase Cell Cycle Checkpointsmedicine.anatomical_structureComplementary and alternative medicineApoptosisCell cultureCaspasesbiology.proteinMolecular MedicineReactive Oxygen SpeciesJournal of Natural Products
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Lovastatin causes sensitization of HeLa cells to ionizing radiation‐induced apoptosis by the abrogation of G2 blockage

2003

To investigate the effect of inhibition of Ras/Rho-regulated signalling by 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) on radiation-induced cell killing and apoptosis.Different human cell lines were pretreated or not with lovastatin before exposure to gamma-rays. Afterwards, radiation-induced cell killing, formation and repair of double-strand breaks, activation of radiation-inducible signal mechanisms (i.e. p53, p21, extracellular-signal-related kinase (ERK), NF-kappaB), changes in cell cycle progression and apoptosis were analysed.As shown by a colony formation assay, lovastatin sensitized HeLa cells to gamma-radiation-induced cell killing. The lovastati…

Cyclin-Dependent Kinase Inhibitor p21G2 PhaseMAPK/ERK pathwayApoptosisBiologyHeLaCyclinspolycyclic compoundsmedicineHumansRadiology Nuclear Medicine and imagingLovastatinSensitizationRadiological and Ultrasound TechnologyKinaseNF-kappa Bnutritional and metabolic diseasesCell cyclebiology.organism_classificationCell biologyCell killingmedicine.anatomical_structureGamma RaysApoptosislipids (amino acids peptides and proteins)LovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsMitogen-Activated Protein KinasesTumor Suppressor Protein p53DNA DamageHeLa Cellsmedicine.drugInternational Journal of Radiation Biology
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Benzo[a]pyrene represses DNA repair through altered E2F1/E2F4 function marking an early event in DNA damage-induced cellular senescence

2020

AbstractTranscriptional regulation of DNA repair is of outmost importance for the restoration of DNA integrity upon genotoxic stress. Here we report that the potent environmental carcinogen benzo[a]pyrene (B[a]P) activates a cellular DNA damage response resulting in transcriptional repression of mismatch repair (MMR) genes (MSH2, MSH6, EXO1) and of RAD51, the central homologous recombination repair (HR) component, ultimately leading to downregulation of MMR and HR. B[a]P-induced gene repression is caused by abrogated E2F1 signalling. This occurs through proteasomal degradation of E2F1 in G2-arrested cells and downregulation of E2F1 mRNA expression in G1-arrested cells. Repression of E2F1-me…

Cyclin-Dependent Kinase Inhibitor p21SenescenceAcademicSubjects/SCI00010DNA repairDNA damageRAD51E2F4 Transcription FactorBiologyDNA Mismatch Repair03 medical and health sciences0302 clinical medicineCell Line TumorBenzo(a)pyreneGeneticsHumansCellular SenescenceCell Line Transformed030304 developmental biology0303 health sciencesGene regulation Chromatin and EpigeneticsRecombinational DNA RepairEpithelial CellsKv Channel-Interacting ProteinsCell Cycle CheckpointsDNAFibroblastsCell biologyDNA-Binding ProteinsRepressor ProteinsMSH6DNA Repair EnzymesExodeoxyribonucleasesMutS Homolog 2 ProteinGamma RaysMSH2030220 oncology & carcinogenesisCarcinogensMCF-7 CellsDNA mismatch repairRad51 RecombinaseCell agingE2F1 Transcription FactorDNA DamageSignal TransductionNucleic Acids Research
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The role of reactive oxygen species and subsequent DNA-damage response in the emergence of resistance towards resveratrol in colon cancer models

2014

AbstractIn spite of the novel strategies to treat colon cancer, mortality rates associated with this disease remain consistently high. Tumour recurrence has been linked to the induction of resistance towards chemotherapy that involves cellular events that enable cancer cells to escape cell death. Treatment of colon cancer mainly implicates direct or indirect DNA-damaging agents and increased repair or tolerances towards subsequent lesions contribute to generate resistant populations. Resveratrol (RSV), a potent chemosensitising polyphenol, might share common properties with chemotherapeutic drugs through its indirect DNA-damaging effects reported in vitro. In this study, we investigated how…

Cyclin-Dependent Kinase Inhibitor p21SenescenceCancer ResearchProgrammed cell deathColonDNA damageColorectal cancerImmunologyApoptosisBiologyResveratrolS PhaseHistonesPolyploidyCellular and Molecular Neurosciencechemistry.chemical_compoundCell Line TumorStilbenesmedicineAnimalsHumansCHEK1Cyclin-Dependent Kinase Inhibitor p16Cell Biologymedicine.diseaseAntineoplastic Agents PhytogenicRatsGene Expression Regulation NeoplasticCheckpoint Kinase 2chemistryDrug Resistance NeoplasmResveratrolApoptosisCheckpoint Kinase 1Cancer cellImmunologyCancer researchOriginal ArticleTumor Suppressor Protein p53Reactive Oxygen SpeciesProtein KinasesDNA DamageSignal TransductionCell Death & Disease
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Ultrastructural and histochemical analysis reveals ethylene-induced responses underlying reduced peel collapse in detached citrus fruit

2010

Fruits from many citrus cultivars develop depressed areas in the flavedo (outer part of the peel) and albedo (inner part) following detachment. Although ultrastructural analysis may provide important information about multiple plant responses to stresses and external stimuli at the cell and tissue levels, and despite the proved efficacy of ethylene in reducing peel damage in citrus fruit, cytological responses of this horticultural crop to protective ethylene concentrations have not yet been reported. We show that applying high ethylene levels (2 mu L L(-1) for 14 days) causes sublethal stress as it favored the alteration of cuticle, vacuole, middle lamella and primary wall, especially in t…

CyclopropanesCitrusHistologyEthylenefood.ingredientPectinStarchCuticleBOTANICAVacuoleBiologyPolysaccharideElectron Microscopy Service of the UPVchemistry.chemical_compoundfoodMicroscopy Electron TransmissionPolysaccharidesBotanyInstrumentationMiddle lamellachemistry.chemical_classificationBIOLOGIA VEGETALfood and beveragesStarchEthylenesCell ultrastructurePectinMedical Laboratory TechnologyHorticulturechemistryFruitPeel damageUltrastructureAnatomyCross-protection
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Nuclear Translocation of Mismatch Repair Proteins MSH2 and MSH6 as a Response of Cells to Alkylating Agents

2000

Mammalian mismatch repair has been implicated in mismatch correction, the prevention of mutagenesis and cancer, and the induction of genotoxicity and apoptosis. Here, we show that treatment of cells specifically with agents inducing O(6)-methylguanine in DNA, such as N-methyl-N'-nitro-N-nitrosoguanidine and N-methyl-N-nitrosourea, elevates the level of MSH2 and MSH6 and increases GT mismatch binding activity in the nucleus. This inducible response occurs immediately after alkylation, is long-lasting and dose-dependent, and results from translocation of the preformed MutSalpha complex (composed of MSH2 and MSH6) from the cytoplasm into the nucleus. It is not caused by an increase in MSH2 gen…

CytoplasmDNA RepairBase Pair MismatchRNA StabilityChromosomal translocationmedicine.disease_causeBiochemistrychemistry.chemical_compoundMismatch Repair Endonuclease PMS2Adenosine TriphosphatasesNuclear ProteinsMethylnitrosoureaNeoplasm ProteinsDNA-Binding ProteinsMutS Homolog 2 ProteinDNA mismatch repairMutL Protein Homolog 1Protein BindingAlkylating AgentsMethylnitronitrosoguanidinecongenital hereditary and neonatal diseases and abnormalitiesGuanineActive Transport Cell NucleusBiologyCell LineO(6)-Methylguanine-DNA MethyltransferaseProto-Oncogene ProteinsDNA Repair ProteinmedicineHumansRNA MessengerneoplasmsMolecular BiologyAdaptor Proteins Signal TransducingCell NucleusMutagenesisnutritional and metabolic diseasesDNACell BiologyDNA MethylationMolecular biologydigestive system diseasesMSH6DNA Repair EnzymesGene Expression RegulationchemistryMSH2Carrier ProteinsGenotoxicityDNADNA DamageHeLa CellsJournal of Biological Chemistry
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