Search results for " Mismatch"

showing 10 items of 140 documents

Photovoltaic electricity scenario analysis in urban contests: an Italian case study

2012

Abstract This paper shows a methodology for the assessment of the photovoltaic potential in urban areas using Google Earth™ tool that provides either satellite images of the roofs of buildings or their number of floors by means of the Street View function. The applicability of the methodology has been tested on a selected urban area of the city of Palermo in the South of Italy. After classifying roofs according to the shape, orientation and pitch of buildings with different morphologies, the share of energy generated by the installable PV systems was evaluated with regard to the number of floors. Moreover the coverage of the electricity demand was investigated on the basis of the consumptio…

Consumption (economics)Engineeringgeographygeography.geographical_feature_categorySettore ING-IND/11 - Fisica Tecnica AmbientaleRenewable Energy Sustainability and the Environmentbusiness.industrymedia_common.quotation_subjectPhotovoltaic systemPhotovoltaic generation Cover factor MismatchEnvironmental economicsUrban areaCivil engineeringIncentiveProduction (economics)Scenario analysisElectricitybusinessFunction (engineering)media_common
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Automated Synthesis of Application-layer Connectors from Automata-based Specifications

2019

Abstract Ubiquitous and Pervasive Computing, and the Internet of Things, promote dynamic interaction among heterogeneous systems. To achieve this vision, interoperability among heterogeneous systems represents a key enabler, and mediators are often built to solve protocol mismatches. Many approaches propose the synthesis of mediators. Unfortunately, a rigorous characterization of the concept of interoperability is still lacking, hence making hard to assess their applicability and soundness. In this paper, we provide a framework for the synthesis of mediators that allows us to: (i) characterize the conditions for the mediator existence and correctness; and (ii) establish the applicability bo…

CorrectnessUbiquitous computingGeneral Computer ScienceComputer Networks and CommunicationsComputer scienceDistributed computingInteroperability0102 computer and information sciences02 engineering and technology01 natural sciencesHeterogeneous ApplicationsTheoretical Computer Science020204 information systems0202 electrical engineering electronic engineering information engineeringProtocol MismatchesCommunication & CoordinationProtocol (object-oriented programming)Automated Mediator SynthesisSoundnessApplied MathematicsAutomated Mediator Synthesis Interoperability Protocols Heterogeneous Applications Communication & Coordination Protocol MismatchesInteroperabilityApplication layerAutomatonComputational Theory and Mathematics010201 computation theory & mathematicsKey (cryptography)Protocols
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Una tipología de desajustes entre competencias y educación utilizando un análisis comparativo entre países

2015

This paper aims to discuss the value of the diplomas and the situation of downgrading on the labour market. Its novelty is to compare skills both acquired and required in employment, using a self - assessment carried out by young higher education graduates a cross nine countries of Europe, Japan and Canada. More precisely, we illustrate the incidences of diploma and skill mismatches using three higher education graduate surveys, two international surveys (CHEERS, REFLEX) and a Canadian survey (NGS). We define possible over - education and skill mismatches and then present an empirical typology to show the most frequent cases of mismatches. The ideal situation which corresponds to a perfect …

Cross-national comparison incidences higher education graduate Europe Over - education[SHS.EDU] Humanities and Social Sciences/Education[ SHS.EDU ] Humanities and Social Sciences/EducationJapan downgrading on the labour market Value of the diploma Canada skill mismatches diploma 
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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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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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Alterations of DNA Repair in Melanoma Cell Lines Resistant to Cisplatin, Fotemustine, or Etoposide

2000

Resistance to chemotherapy is a common phenomenon in malignant melanoma. In order to assess the role of altered DNA repair in chemoresistant melanoma, we investigated different DNA repair pathways in one parental human melanoma line (MeWo) and in sublines of MeWo selected in vitro for drug resistance against four commonly used drugs (cisplatin, fotemustine, etoposide, and vindesine). Host cell reactivation assays with the plasmid pRSVcat were used to assess processing of different DNA lesions. With ultraviolet-irradiated plasmids, no significant differences were found, indicating a normal (nucleotide excision) repair of DNA photoproducts. With singlet oxygen-treated plasmid, the fotemustine…

DNA RepairUltraviolet RaysDNA repairDNA damageDrug ResistanceAntineoplastic AgentsDermatologyBiologyHost-Cell Reactivationbase excision repairBiochemistryNitrosourea Compounds03 medical and health sciencesOrganophosphorus Compounds0302 clinical medicineTumor Cells CulturedmedicineHumansMelanomaMolecular BiologyEtoposide030304 developmental biology0303 health scienceschemoresistanceMicrosatellite instabilityDNA NeoplasmBase excision repairCell BiologyDNA repair protein XRCC4nucleotide excision repairmedicine.diseaseAntineoplastic Agents PhytogenicMolecular biology3. Good healthOxygenmismatch repair030220 oncology & carcinogenesisDNA mismatch repairCisplatinMicrosatellite RepeatsNucleotide excision repairJournal of Investigative Dermatology
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Mechanisms and consequences of methylating agent-induced SCEs and chromosomal aberrations: a long road traveled and still a far way to go.

2003

Since the milestone work of Evans and Scott, demonstrating the replication dependence of alkylation-induced aberrations, and Obe and Natarajan, pointing to the critical role of DNA double-strand breaks (DSBs) as the ultimate trigger of aberrations, the field has grown extensively. A notable example is the identification of DNA methylation lesions provoking chromosome breakage (clastogenic) effects, which made it possible to model clastogenic pathways evoked by genotoxins. Experiments with repair-deficient mutants and transgenic cell lines revealed both O<sup>6</sup>-methylguanine (O<sup>6</sup>MeG) and N- methylpurines as critical lesions. For S<sub>N</sub&g…

DNA ReplicationAlkylating AgentsGuanineDNA RepairDNA damageDNA repairBase Pair MismatchApoptosisBiologyMethylationLesionAnimals Genetically ModifiedMiceO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeGeneticsmedicineAnimalsHumansPoint MutationAP siteMolecular BiologyGenetics (clinical)Chromosome AberrationsRecombination GeneticGuanosineModels GeneticCell CycleDNA replicationDNAFibroblastsMolecular biologyCell killingCell Transformation NeoplasticCancer researchDNA mismatch repairChromosome breakagemedicine.symptomSister Chromatid ExchangeDNA DamageMutagensCytogenetic and genome research
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Chromosomal instability, reproductive cell death and apoptosis induced by O6-methylguanine in Mex−, Mex+ and methylation-tolerant mismatch repair com…

1998

O6-Methylguanine (O6-MeG) is induced in DNA by methylating environmental carcinogens and various cytostatic drugs. It is repaired by O6-methylguanine-DNA methyltransferase (MGMT). If not repaired prior to replication, the lesion generates gene mutations and leads to cell death, sister chromatid exchanges (SCEs), chromosomal aberrations and malignant transformation. To address the question of how O6-MeG is transformed into genotoxic effects, isogenic Chinese hamster cell lines either not expressing MGMT (phenotypically Mex-), expressing MGMT (Mex+) or exhibiting the tolerance phenotype (Mex-, methylation resistant) were compared as to their clastogenic response. Mex- cells were more sensitiv…

DNA ReplicationMethylnitronitrosoguanidineGuanineDNA RepairDNA damageHealth Toxicology and MutagenesisDrug ResistanceApoptosisCHO CellsGene mutationBiologyChromosomesDNA AdductsO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeChromosome instabilityGeneticsAnimalsSister chromatidsMolecular BiologyMitosisChromosome AberrationsCell DeathModels GeneticMutagenicity TestsDNA replicationDNA MethylationMolecular biologyDNA methylationDNA mismatch repairSister Chromatid ExchangeMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Processing of O6-methylguanine into DNA double-strand breaks requires two rounds of replication whereas apoptosis is also induced in subsequent cell …

2009

The DNA adduct O(6)-methylguanine (O(6)MeG) induced by environmental genotoxins and anticancer drugs is a highly mutagenic, genotoxic and apoptotic lesion. Apoptosis induced by O(6)MeG requires mismatch repair (MMR) and proliferation. Models of O(6)MeG-triggered cell death postulate that O(6)MeG/T mispairs activate MMR giving rise to either direct genotoxic signaling or secondary lesions that trigger apoptotic signaling in the 2(nd) replication cycle. To test these hypotheses, we used a highly synchronized cell system competent and deficient for the repair of O(6)MeG adducts, which were induced by the S(N)1 methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). We show that DNA doub…

DNA ReplicationProgrammed cell deathMethylnitronitrosoguanidineCell cycle checkpointGuanineDNA repairBlotting WesternSuccinimidesApoptosisCHO CellsBiologychemistry.chemical_compoundO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeDNA adductAnimalsDNA Breaks Double-StrandedMolecular BiologyCell CycleCell BiologyCell cycleFlow CytometryFluoresceinsMolecular biologyCell biologychemistryMicroscopy FluorescenceApoptosisDNA mismatch repairDNADevelopmental BiologyCell cycle (Georgetown, Tex.)
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The Translesion Polymerase Rev3L in the Tolerance of Alkylating Anticancer Drugs

2009

Temozolomide and fotemustine, representing methylating and chloroethylating agents, respectively, are used in the treatment of glioma and malignant melanoma. Because chemoresistance of these tumors is a common phenomenon, identification of the underlying mechanisms is needed. Here we show that Rev3L, the catalytic subunit of the translesion DNA polymerase zeta, mediates resistance to both temozolomide and fotemustine. Rev3L knockout cells are hypersensitive to both agents. It is remarkable that cells heterozygous for Rev3L showed an intermediate sensitivity. Rev3L is not involved in the tolerance of the toxic O6-methylguanine lesion. However, a possible role of Rev3L in the tolerance of O6-…

DNA damageApoptosisDNA-Directed DNA PolymeraseBiologyNitrosourea CompoundsCell LineMiceOrganophosphorus CompoundsREV3LTemozolomidemedicineAnimalsAP siteAntineoplastic Agents AlkylatingPolymeraseMice KnockoutPharmacologyTemozolomideBase excision repairFlow CytometryMolecular biologyDNA-Binding ProteinsDacarbazineMicroscopy FluorescenceCancer researchbiology.proteinMolecular MedicineFotemustineDNA mismatch repairDrug Screening Assays AntitumorDNA Damagemedicine.drugMolecular Pharmacology
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