Search results for "MESH: Humans"

showing 10 items of 211 documents

The stable repression of mesenchymal program is required for hepatocyte identity: A novel role for hepatocyte nuclear factor 4α

2011

The concept that cellular terminal differentiation is stably maintained once development is complete has been questioned by numerous observations showing that differentiated epithelium may undergo an epithelial-to-mesenchymal transition (EMT) program. EMT and the reverse process, mesenchymal-to-epithelial transition (MET), are typical events of development, tissue repair, and tumor progression. In this study, we aimed to clarify the molecular mechanisms underlying these phenotypic conversions in hepatocytes. Hepatocyte nuclear factor 4α (HNF4α) was overexpressed in different hepatocyte cell lines and the resulting gene expression profile was determined by real-time quantitative polymerase…

Transcription FactorCellular differentiationMESH: Mice KnockoutMESH: HepatocytesMesodermMice0302 clinical medicineMESH: Liver NeoplasmsMESH: AnimalsHepatocyteHepatocyte Nuclear Factor 1-alphaMESH: Carcinoma HepatocellularRegulator geneHepatocyte differentiationMice KnockoutMESH: Mesoderm0303 health sciencesLiver NeoplasmsCell DifferentiationMESH: Transcription FactorsCell biologyHepatocyte nuclear factorsPhenotypeMESH: Models AnimalHepatocyte Nuclear Factor 4MESH: Epithelial CellsLiver Neoplasm030220 oncology & carcinogenesisModels AnimalMESH: Hepatocyte Nuclear Factor 4HumanMESH: Cell DifferentiationMESH: Cell Line TumorCarcinoma Hepatocellular[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyMESH: PhenotypeArticle03 medical and health scienceshepatocyte; mesenchymal program; SnailCell Line TumorAnimalsHumansMESH: Hepatocyte Nuclear Factor 1-alphaMESH: MiceTranscription factorAnimals; Carcinoma Hepatocellular; Cell Differentiation; Cell Line Tumor; Epithelial Cells; Hepatocyte Nuclear Factor 1-alpha; Hepatocyte Nuclear Factor 4; Hepatocytes; Humans; Liver Neoplasms; Mesoderm; Mice; Mice Knockout; Models Animal; Phenotype; Snail Family Transcription Factors; Transcription Factors; Hepatology030304 developmental biologyEpithelial CellMESH: HumansHepatologyAnimalMesenchymal stem cellEpithelial CellsSnail Family Transcription FactorMolecular biologyHepatocyte nuclear factor 4HepatocytesSnail Family Transcription FactorsChromatin immunoprecipitationTranscription Factors
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Analysis of integrated virological and epidemiological reports of norovirus outbreaks collected within the Foodborne Viruses in Europe network from 1…

2008

ABSTRACT The Foodborne Viruses in Europe network has developed integrated epidemiological and virological outbreak reporting with aggregation and sharing of data through a joint database. We analyzed data from reported outbreaks of norovirus (NoV)-caused gastroenteritis from 13 European countries (July 2001 to July 2006) for trends in time and indications of different epidemiology of genotypes and variants. Of the 13 countries participating in this surveillance network, 11 were capable of collecting integrated epidemiological and virological surveillance data and 10 countries reported outbreaks throughout the entire period. Large differences in the numbers and rates of reported outbreaks pe…

Veterinary medicineEpidemiologyMESH : Genotypemedicine.disease_causeDisease OutbreaksFoodborne DiseasesMESH: GenotypeEpidemiologyMedicineMESH: Disease OutbreaksMESH: Caliciviridae InfectionsCaliciviridae Infections0303 health sciencesFood poisoningbiologyTransmission (medicine)Incidence (epidemiology)Gastroenteritis3. Good healthEuropeMESH : GastroenteritisDisease Notification[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/VirologyMESH : Caliciviridae InfectionsMicrobiology (medical)MESH: Norovirusmedicine.medical_specialtyGenotypeMESH: Disease NotificationMESH : Europe[ SDV.MP.VIR ] Life Sciences [q-bio]/Microbiology and Parasitology/VirologyMESH: Multivariate Analysis03 medical and health sciencesEnvironmental healthHumansMESH : Disease OutbreaksMESH : Foodborne DiseasesMESH: Foodborne DiseasesDisease Notification030304 developmental biologyMESH: Humans030306 microbiologybusiness.industryMESH : NorovirusNorovirusMESH : HumansOutbreakMESH : Multivariate AnalysisMESH : Disease Notificationmedicine.diseasebiology.organism_classificationCaliciviridaeMESH: GastroenteritisMultivariate AnalysisNorovirusMESH: Europebusiness
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Wee1 inhibition potentiates Wip1-dependent p53-negative tumor cell death during chemotherapy

2016

AbstractInactivation of p53 found in more than half of human cancers is often associated with increased tumor resistance to anti-cancer therapy. We have previously shown that overexpression of the phosphatase Wip1 in p53-negative tumors sensitizes them to chemotherapeutic agents, while protecting normal tissues from the side effects of anti-cancer treatment. In this study, we decided to search for kinases that prevent Wip1-mediated sensitization of cancer cells, thereby interfering with efficacy of genotoxic anti-cancer drugs. To this end, we performed a flow cytometry-based screening in order to identify kinases that regulated the levels of γH2AX, which were used as readout. Another criter…

Wip1ApoptosisCell Cycle ProteinsPharmacologyMESH: G2 Phase Cell Cycle CheckpointsHistonesMESH : PhosphorylationMiceMESH : Cell Cycle ProteinsMESH: AnimalsMESH: Tumor Suppressor Protein p53MESH: HistonesKinaseTp53 mutationsMESH : Mice Transgenic3. Good healthProtein Phosphatase 2CSurvival RateMESH : Antineoplastic AgentsH2ax phosphorylationP53 activationMESH: Protein Phosphatase 2CRNA InterferenceMESH : Colorectal NeoplasmsMESH : Carrier ProteinsHistone H2axMESH: MitochondriaImmunologyHuman fibroblastsMESH: Carrier ProteinsAntineoplastic AgentsMESH: Protein-Tyrosine KinasesMESH: Protein-Serine-Threonine KinasesMESH : Cisplatin03 medical and health sciencesMESH: Cell Cycle ProteinsGenotoxic stressMESH : Protein-Tyrosine KinasesHumansMESH : HistonesAnticancer TherapyMESH: DNA DamageCisplatinMESH: HumansMESH: Phosphorylation[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH : HumansMESH : Nuclear Proteins030104 developmental biologyCancer cellMESH: Antineoplastic AgentsCisplatinCarrier ProteinsMESH: Nuclear ProteinsMESH : ApoptosisDna-damage response0301 basic medicineCancer ResearchMESH: Caspase 3MESH : Caspase 3PhosphorylationCytotoxicityMESH : DNA DamageSensitizationmedicine.diagnostic_testCaspase 3Nuclear ProteinsProtein-Tyrosine KinasesMESH : Survival RateMitochondriaG2 Phase Cell Cycle CheckpointsWee1medicine.anatomical_structureMESH : Protein Phosphatase 2COriginal ArticleMESH : MitochondriaColorectal Neoplasmsmedicine.drugMESH : Protein-Serine-Threonine KinasesMESH: Cell Line TumorMESH: Survival RateMESH: Mice TransgenicMESH: RNA InterferencePhosphataseMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesFlow cytometryCellular and Molecular NeuroscienceCell Line TumorMESH : MicemedicineAnimalsMESH: MiceMESH : Cell Line TumorMESH: ApoptosisCell BiologyMESH : Tumor Suppressor Protein p53MESH: CisplatinCancer researchbiology.proteinMESH : AnimalsMESH : G2 Phase Cell Cycle CheckpointsMESH : RNA InterferenceTumor Suppressor Protein p53MESH: Colorectal NeoplasmsDNA DamageCell Death & Disease
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Distinct Clones of Yersinia pestis Caused the Black Death

2010

From AD 1347 to AD 1353, the Black Death killed tens of millions of people in Europe, leaving misery and devastation in its wake, with successive epidemics ravaging the continent until the 18th century. The etiology of this disease has remained highly controversial, ranging from claims based on genetics and the historical descriptions of symptoms that it was caused by Yersinia pestis to conclusions that it must have been caused by other pathogens. It has also been disputed whether plague had the same etiology in northern and southern Europe. Here we identified DNA and protein signatures specific for Y. pestis in human skeletons from mass graves in northern, central and southern Europe that …

Yersinia pestis[SDV]Life Sciences [q-bio]Sequence HomologyDiseaseMESH: Base SequenceMESH: Genetic Markers[SHS]Humanities and Social SciencesDisease OutbreaksInfectious Diseases/Bacterial InfectionsMESH: GenotypeGenotypeMass ScreeningBiology (General)MESH: Disease OutbreaksMESH: PhylogenyCladePhylogenyGenetics0303 health sciencesMicrobiology/Microbial Evolution and GenomicsbiologyClones; Yersinia pestis; Black DeathBacterialGenetics and Genomics/Microbial Evolution and Genomics3. Good healthEuropeEvolutionary Biology/Human EvolutionInfectious DiseasesResearch ArticleDNA BacterialGenetic MarkersGenotypeQH301-705.5Molecular Sequence DataImmunologyMESH: Yersinia pestisZoologyMolecular Biology/Molecular EvolutionPlague (disease)MESH: PlagueMESH: Sequence Homology Nucleic AcidMicrobiologyNO03 medical and health sciencesPhylogeneticsSequence Homology Nucleic AcidVirologyGeneticsHumansMESH: Mass ScreeningEpidemicsMolecular BiologyMESH: EpidemicsMass screening030304 developmental biologyPlagueEvolutionary BiologyMESH: HumansMESH: Molecular Sequence DataNucleic AcidBase Sequence030306 microbiologyGenetics and GenomicsDNARC581-607biology.organism_classificationMESH: DNA BacterialYersinia pestisBase Sequence; DNA Bacterial; Disease Outbreaks; Epidemics; Europe; Genetic Markers; Genotype; Humans; Mass Screening; Molecular Sequence Data; Phylogeny; Plague; Sequence Homology Nucleic Acid; Yersinia pestisEtiologyParasitologyMESH: EuropeImmunologic diseases. Allergy
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Cyclo-oxygenase isoenzymes. How recent findings affect thinking about nonsteroidal anti-inflammatory drugs

1997

International audience; The discovery of at least 2 cyclo-oxygenase (COX) isoenzymes, referred to as COX-1 and COX-2, has updated our knowledge of nonsteroidal anti-inflammatory drugs (NSAIDs). This has lead investigators to reconsider what can be awaited from this class of drugs. The 2 COX isoenzymes share structural and enzymatic similarities, but are specifically regulated at the molecular level and may be distinguished apart in their functions, although some physiological overlap between them does occur. The major goal in developing selective COX inhibitors is to improve NSAID tolerability. Classic NSAIDs preferentially inhibit COX-1 in vitro, but it appears hazardous to judge their gas…

[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionMESH: Prostaglandin-Endoperoxide SynthasesAnti-Inflammatory AgentsPharmacologyNabumetoneMESH: Cyclooxygenase InhibitorsPharmacotherapymedicineMESH : Anti-Inflammatory Agents Non-SteroidalAnimalsHumansPharmacology (medical)Cyclooxygenase InhibitorsMESH: AnimalsAdverse effectMESH: HumansMESH : Prostaglandin-Endoperoxide Synthasesbusiness.industryMESH : HumansAnti-Inflammatory Agents Non-SteroidalMESH : Cyclooxygenase InhibitorsMESH: Anti-Inflammatory Agents Non-SteroidalClinical trial[SDV.AEN] Life Sciences [q-bio]/Food and NutritionMeloxicamTolerabilityProstaglandin-Endoperoxide SynthasesMESH : AnimalsCyclo-oxygenaseNon-Steroidalbusiness[SDV.AEN]Life Sciences [q-bio]/Food and NutritionNimesulidemedicine.drug
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The Urban Exposome during Pregnancy and Its Socioeconomic Determinants

2018

Background: The urban exposome is the set of environmental factors that are experienced in the outdoor urban environment and that may influence child development. Objective: The authors’ goal was to describe the urban exposome among European pregnant women and understand its socioeconomic determinants. Methods: Using geographic information systems, remote sensing and spatio-temporal modeling we estimated exposure during pregnancy to 28 environmental indicators in almost 30,000 women from six population-based birth cohorts, in nine urban areas from across Europe. Exposures included meteorological factors, air pollutants, traffic noise, traffic indicators, natural space, the built environment…

[SDE] Environmental SciencesUrban PopulationHealth Toxicology and Mutagenesis05 Environmental SciencesNEIGHBORHOOD WALKABILITY010501 environmental sciencesToxicology01 natural sciences0302 clinical medicineUSE REGRESSION-MODELS11. Sustainability030212 general & internal medicineNITROGEN-DIOXIDE11 Medical And Health Sciences3. Good healthPeer reviewEuropeMESH: Urban PopulationGeographyGREEN SPACESMESH: Environmental PollutantsMESH: Young Adult[SDE]Environmental SciencesENVIRONMENTAL JUSTICEEnvironmental PollutantsFemaleAdultExposomemedicine.medical_specialtyMESH: Socioeconomic FactorsAdolescentMESH: Environmental ExposureYoung Adult03 medical and health sciencesEnvironmental healthmedicineMESH: CitiesHumansCitiesSocioeconomic status0105 earth and related environmental sciencesEnvironmental justiceMESH: AdolescentPregnancyMESH: HumansLand useLAND-USEResearchPublic healthPublic Health Environmental and Occupational HealthMESH: AdultEnvironmental Exposuremedicine.diseaseChild developmentAMBIENT AIR-POLLUTIONROAD TRAFFIC NOISERESIDENTIAL EXPOSURESocioeconomic Factors[SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie13. Climate actionCOHORT PROFILE[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologieMESH: EuropeMESH: Female
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Factors related to the relative survival of patients with diffuse large B-cell lymphoma in a population-based study in France: does socio-economic st…

2017

IF 7.702; International audience; The survival of patients with diffuse large B-cell lymphoma has increased during the last decade as a result of addition of anti-CD20 to anthracycline-based chemotherapy. Although the trend is encouraging, there are persistent differences in survival within and between the USA and European countries suggesting that non-biological factors play a role. Our aim was to investigate the influence of such factors on relative survival of patients with diffuse large B-cell lymphoma. We conducted a retrospective, multicenter, registry-based study in France on 1165 incident cases of diffuse large B-cell lymphoma between 2002 and 2008. Relative survival analyses were p…

[SDV.MHEP.HEM] Life Sciences [q-bio]/Human health and pathology/HematologyMale0301 basic medicinePediatricsMultivariate analysisMESH: RegistriesMESH : AgedMESH: ComorbidityComorbidityMESH : Lymphoma Large B-Cell DiffuseMESH: Aged 80 and over0302 clinical medicineInternational Prognostic IndexMESH : ChildMESH: ChildMESH : Population Surveillance[ SDV.MHEP.HEM ] Life Sciences [q-bio]/Human health and pathology/HematologyMESH : FemaleRegistriesYoung adultChildAged 80 and overMESH: AgedMESH: Middle AgedMESH : PrognosisRelative survivalMESH: Patient Outcome Assessment[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyArticlesHematologyMiddle AgedMESH : AdultPrognosisMESH : Patient Outcome Assessment3. Good healthMESH: Young AdultPopulation SurveillanceMESH: Survival Analysis030220 oncology & carcinogenesisMESH : ComorbidityMarital statusFemaleFranceLymphoma Large B-Cell DiffuseNon-Hodgkin LeukemiaAdultmedicine.medical_specialtyAdolescentMESH : MaleMESH: Factor Analysis StatisticalMESH : Young AdultMESH : Factor Analysis StatisticalMESH: PrognosisMESH: Population SurveillanceMESH: Social ClassYoung Adult03 medical and health sciencesMESH : AdolescentInternal medicineMESH : Social ClassmedicineHumansMESH : Middle AgedMESH : Aged 80 and overMESH : FranceSurvival analysisAgedMESH: AdolescentMESH: Humansbusiness.industryMESH : HumansMESH: Adultmedicine.diseaseSurvival AnalysisComorbidityMESH: MalePatient Outcome AssessmentMESH: France030104 developmental biologySocial ClassMESH: Lymphoma Large B-Cell DiffuseMESH : Survival AnalysisFactor Analysis StatisticalbusinessMESH: FemaleDiffuse large B-cell lymphomaMESH : RegistriesHaematologica
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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

2016

Seuls les 100 premiers auteurs dont les auteurs INRA ont été entrés dans la notice. La liste complète des auteurs et de leurs affiliations est accessible sur la publication.; International audience; In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues…

[SDV]Life Sciences [q-bio]autophagosomeReview Articleddc:616.07stressstreLC3MESH: AnimalsSettore MED/49 - Scienze Tecniche Dietetiche ApplicateSettore BIO/06 - Anatomia Comparata E Citologiachaperone-mediated autophagyComputingMilieux_MISCELLANEOUSSettore BIO/11Pharmacology. TherapySettore BIO/13standards [Biological Assay]autolysosomeMESH: Autophagy*/physiologylysosomemethods [Biological Assay]Biological AssaySettore BIO/17 - ISTOLOGIAErratumHumanBiochemistry & Molecular BiologySettore BIO/06physiology [Autophagy]Chaperonemediated autophagy[SDV.BC]Life Sciences [q-bio]/Cellular BiologyNOautophagy guidelines molecular biology ultrastructureautolysosome; autophagosome; chaperone-mediated autophagy; flux; LC3; lysosome; macroautophagy; phagophore; stress; vacuoleMESH: Biological Assay/methodsMESH: Computer Simulationddc:570Autolysosome Autophagosome Chaperonemediated autophagy Flux LC3 Lysosome Macroautophagy Phagophore Stress VacuoleAutophagyAnimalsHumansComputer SimulationSettore BIO/10ddc:612BiologyphagophoreMESH: HumansvacuoleAnimalLC3; autolysosome; autophagosome; chaperone-mediated autophagy; flux; lysosome; macroautophagy; phagophore; stress; vacuole; Animals; Biological Assay; Computer Simulation; Humans; Autophagy0601 Biochemistry And Cell BiologyfluxmacroautophagyMESH: Biological Assay/standards*Human medicineLC3; autolysosome; autophagosome; chaperone-mediated autophagy; flux; lysosome; macroautophagy; phagophore; stress; vacuole
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Autophagy

2012

Klionsky, Daniel J. et al.

autophagy assays[SDV]Life Sciences [q-bio]AutolysosomeAutophagosome maturationautophagosomeBioinformaticsstressChaperone-mediated autophagyModelsLC3MESH: Animalsguidelinesautolysosome autophagosome flux LC3 lysosome phagophore stress vacuoleSettore BIO/06 - Anatomia Comparata E CitologiaComputingMilieux_MISCELLANEOUSSettore BIO/17Autophagy databaseautolysosome3. Good healthddc:540lysosomeEnergy and redox metabolism Mitochondrial medicine [NCMLS 4]methods [Biological Assay]Biological AssaySettore BIO/17 - ISTOLOGIANeuroniMAP1LC3BHumanautophagygenetics [Autophagy]AutofagiaMESH: Autophagy*/genetics[SDV.BC]Life Sciences [q-bio]/Cellular BiologyAutofagia; Neuroni; istologiaBiologyModels BiologicalLC3; autolysosome; autophagosome; flux; lysosome; phagophore; stress; vacuoleddc:570AutophagyAnimalsHumansAutophagy-Related Protein 7[SDV.BC] Life Sciences [q-bio]/Cellular BiologyBiological Assay/methodsMolecular BiologyBiologyAutophagy; guidelines; autophagy assaysistologiaphagophoreMESH: HumansAnimals; Biological Assay; Humans; Models Biological; AutophagyvacuoleAnimal[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH: Models BiologicalPathogenesis and modulation of inflammation Infection and autoimmunity [N4i 1]Cell BiologyBiologicalAutophagy/geneticsfluxAutophagosome membraneAutophagy Protein 5Human medicineMESH: Biological Assay/methods*Neuroscienceautolysosome; autophagosome; flux; LC3; lysosome; phagophore; stress; vacuoleAutophagy
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A role for peroxisome proliferator-activated receptor gamma in resveratrol-induced colon cancer cell apoptosis.

2014

Scope Resveratrol may function as a chemopreventive agent. A recent clinical study demonstrates a reduction in tumor cell proliferation in colorectal patients receiving repeated oral ingestion of resveratrol. However, gaps remain in our knowledge of the molecular mechanisms by which resveratrol exerts its chemopreventive effect. We have previously demonstrated that resveratrol induces apoptosis in colon cancer cells and that resveratrol can sensitize chemoresistant colon cancer cells to various drugs. Based on its ability to activate peroxisome proliferator-activated receptor gamma (PPARγ) in colon cancer cells, we sought to determine the implication of this nuclear transcription factor in …

endocrine system diseasesColorectal cancerPeroxisome proliferator-activated receptorApoptosisPharmacologyResveratrolresveratrolMESH: ThiazolidinedionesPPAR[ SDV.CAN ] Life Sciences [q-bio]/Cancerchemistry.chemical_compound0302 clinical medicineMESH: StilbenesStilbenesMESH : Cell Proliferation[ SHS.INFO ] Humanities and Social Sciences/Library and information sciencesAnilidesskin and connective tissue diseaseschemistry.chemical_classification0303 health sciencesfood and beveragesCell cycle3. Good healthMESH : ThiazolidinedionesMESH : Colonic Neoplasmscolon cancer030220 oncology & carcinogenesisColonic NeoplasmsS Phase Cell Cycle CheckpointsRosiglitazonehormones hormone substitutes and hormone antagonistsBiotechnologymedicine.drugMESH : PPAR gammaMESH: Cell Line Tumor[SHS.INFO]Humanities and Social Sciences/Library and information sciences[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyMESH: Anilides[SHS.INFO] Humanities and Social Sciences/Library and information sciencesMESH : AnilidesMESH : StilbenesRosiglitazone03 medical and health sciences[SDV.CAN] Life Sciences [q-bio]/CancerCell Line TumorMESH: Cell Proliferationmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[SDV.BC] Life Sciences [q-bio]/Cellular BiologyMESH : S Phase Cell Cycle Checkpoints[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biologypolyphenols030304 developmental biologyCell ProliferationMESH: Colonic NeoplasmsMESH: HumansCell growthMESH : Cell Line Tumor[ SDV.BC ] Life Sciences [q-bio]/Cellular Biologyorganic chemicalsMESH: ApoptosisMESH : Humansmedicine.diseasePPAR gammaMESH: S Phase Cell Cycle CheckpointschemistryMESH: PPAR gammaApoptosisCancer cellThiazolidinedionesMESH : ApoptosisFood Science
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