Search results for "MESH: Phenotype"

showing 3 items of 13 documents

Factors that predict response of patients with hepatitis C virus infection to boceprevir

2012

Background & Aims Little is known about factors associated with a sustained virologic response (SVR) among patients with hepatitis C virus (HCV) infection to treatment with protease inhibitors. Methods Previously untreated patients (from the Serine Protease Inhibitor Therapy 2 [SPRINT-2] trial) and those who did not respond to prior therapy (from the Retreatment with HCV Serine Protease Inhibitor Boceprevir and PegIntron/Rebetol 2 [RESPOND-2] trial) received either a combination of peginterferon and ribavirin for 48 weeks or boceprevir, peginterferon, and ribavirin (triple therapy) after 4 weeks of peginterferon and ribavirin (total treatment duration, 28–48 wk). A good response to interfer…

MaleCirrhosisMESH: Logistic ModelsHepacivirusMESH: Risk AssessmentGastroenterologyPolyethylene GlycolsMESH: Recombinant ProteinsMESH: Genotype0302 clinical medicineOdds RatioProspective StudiesMESH: Treatment OutcomeResponse to Therapy0303 health sciencesMESH: Polymorphism Single NucleotideGastroenterologyvirus diseases3. Good healthMESH: RNA ViralHCVDrug Therapy Combination030211 gastroenterology & hepatologyClinical Trial; Genetic; Prognostic Factors; Response to Therapy; Adult; Antiviral Agents; Biomarkers; Canada; Drug Therapy Combination; Europe; Female; Genotype; Hepacivirus; Hepatitis C; Humans; Interferon-alpha; Interleukins; Logistic Models; Male; Multivariate Analysis; Odds Ratio; Phenotype; Polyethylene Glycols; Polymorphism Single Nucleotide; Proline; Prospective Studies; RNA Viral; Recombinant Proteins; Ribavirin; Risk Assessment; Risk Factors; Time Factors; Treatment Outcome; United States; Viral Load; GastroenterologyViral loadmedicine.medical_specialtyMESH: InterleukinsGenotypeProlineInterferon alpha-2MESH: PhenotypeAntiviral AgentsRisk Assessment03 medical and health sciencesDrug TherapyGeneticMESH: RibavirinMESH: CanadaBoceprevirHumansPolymorphismMESH: ProlineMESH: HumansPrognostic FactorsInterleukinsMESH: AdultOdds ratiomedicine.diseaseUnited Statesdigestive system diseasesClinical trialLogistic ModelschemistryImmunologyMESH: FemaleBiomarkersTime Factorsmedicine.disease_causechemistry.chemical_compoundRisk FactorsInterferonMESH: Risk FactorsMESH: HepacivirusViralSingle NucleotideViral LoadHepatitis CClinical TrialRecombinant ProteinsEuropePhenotypeTreatment OutcomeCombinationRNA ViralFemaleMESH: Interferon-alphaMESH: Viral Loadmedicine.drugAdultMESH: Antiviral AgentsCanadaHepatitis C virusPolymorphism Single NucleotideMESH: Multivariate AnalysisInternal medicineRibavirinmedicineMESH: United States030304 developmental biologyMESH: Hepatitis CHepatologybusiness.industryRibavirinMESH: Time FactorsMESH: Biological MarkersInterferon-alpha[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH: Prospective StudiesMESH: MaleMESH: Odds RatioMESH: Drug Therapy CombinationMESH: Polyethylene GlycolsMultivariate AnalysisRNAInterferonsMESH: Europebusiness
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The columnar gene vnd is required for tritocerebral neuromere formation during embryonic brain development of Drosophila.

2006

International audience; In Drosophila, evolutionarily conserved transcription factors are required for the specification of neural lineages along the anteroposterior and dorsoventral axes, such as Hox genes for anteroposterior and columnar genes for dorsoventral patterning. In this report, we analyse the role of the columnar patterning gene ventral nervous system defective (vnd) in embryonic brain development. Expression of vnd is observed in specific subsets of cells in all brain neuromeres. Loss-of-function analysis focussed on the tritocerebrum shows that inactivation of vnd results in regionalized axonal patterning defects, which are comparable with the brain phenotype caused by mutatio…

Nervous systemMutantApoptosis0302 clinical medicineMESH: Gene Expression Regulation DevelopmentalDrosophila ProteinsMESH: AnimalsAxonHox geneMESH: MelatoninGenetics0303 health sciencesMESH: Pineal GlandBrainGene Expression Regulation DevelopmentalMESH: Transcription FactorsNeuromerePhenotypeBiological EvolutionCell biologymedicine.anatomical_structureDrosophila melanogasterPhenotypeMESH: Photic StimulationMESH: Body PatterningMESH: MutationMESH: Drosophila ProteinsBiologyMESH: PhenotypeMESH: Drosophila melanogaster03 medical and health sciencesMESH: BrainNeuroblastMESH: EvolutionMESH: Homeodomain ProteinsmedicineAnimalsMESH: Circadian RhythmMolecular Biology030304 developmental biologyBody PatterningHomeodomain ProteinsMESH: HumansMESH: ApoptosisEmbryogenesis[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMESH: LightMutationMESH: SerotoninMESH: Seasons030217 neurology & neurosurgeryDevelopmental BiologyTranscription Factors
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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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