Search results for "model."

showing 10 items of 23664 documents

Protein tyrosine phosphatase 1b deficiency protects against hepatic fibrosis by modulating nadph oxidases

2019

Inflammation is typically associated with the development of fibrosis, cirrhosis and hepatocellular carcinoma. The key role of protein tyrosine phosphatase 1B (PTP1B) in inflammatory responses has focused this study in understanding its implication in liver fibrosis. Here we show that hepatic PTP1B mRNA expression increased after bile duct ligation (BDL), while BDL-induced liver fibrosis was markedly reduced in mice lacking Ptpn1 (PTP1B−/−) as assessed by decreased collagen deposition and α-smooth muscle actin (α-SMA) expression. PTP1B−/− mice also showed a significant increase in mRNA levels of key markers of monocytes recruitment (Cd68, Adgre1 and Ccl2) compared to their wild-type (PTP1B+…

0301 basic medicineLiver CirrhosisMaleClinical BiochemistryGene ExpressionApoptosisBiochemistryMice0302 clinical medicineFibrosisTransforming Growth Factor betaRNA Small Interferinglcsh:QH301-705.5Liver injuryProtein Tyrosine Phosphatase Non-Receptor Type 1lcsh:R5-920NADPH oxidaseProtein tyrosine phosphatase 1BbiologyChemistryNOX4Bile duct ligationImmunohistochemistry3. Good healthNOX1Femalelcsh:Medicine (General)hormones hormone substitutes and hormone antagonistsResearch PaperBone marrow transplantationKupffer CellsLiver fibrosisdigestive systemCell LineBile Acids and Salts03 medical and health sciencesmedicineHepatic Stellate CellsAnimalsInflammationOrganic Chemistrymedicine.diseaseMolecular biologyTransplantationDisease Models Animal030104 developmental biologylcsh:Biology (General)Culture Media ConditionedNADPH oxidasesHepatic stellate cellbiology.proteinHepatocytesHepatic fibrosisReactive Oxygen Species030217 neurology & neurosurgeryBiomarkersRedox Biology
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PI3K inhibition reduces murine and human liver fibrogenesis in precisioncut liver slices

2019

Background: Liver fibrosis results from continuous inflammation and injury. Despite its high prevalence worldwide, no approved antifibrotic therapies exist. Omipalisib is a selective inhibitor of the PI3K/mTOR pathway that controls nutrient metabolism, growth and proliferation. It has shown antifibrotic properties in vitro. While clinical trials for idiopathic pulmonary fibrosis have been initiated, an in-depth preclinical evaluation is lacking. We evaluated omipalisib's effects on fibrogenesis using the ex vivo model of murine and human precision-cut tissue slices (PCTS).Methods: Murine and human liver and jejunum PCTS were incubated with omipalisib up to 10 mu M for 48 h. PI3K pathway act…

0301 basic medicineLiver CirrhosisMalePrecision-cut tissue slicesPROGRESSIONPharmacologyBILIARYBiochemistryPI3KGSK2126458JejunumMicePhosphatidylinositol 3-Kinases0302 clinical medicineAdenosine TriphosphateFibrosisFIBROSIShealth care economics and organizationsPhosphoinositide-3 Kinase InhibitorsSulfonamidesPyridazinesmedicine.anatomical_structureJejunumTARGET030220 oncology & carcinogenesisToxicityQuinolinesPhosphorylationmedicine.symptomATP Binding Cassette Transporter Subfamily BLiver fibrosisEARLY-ONSETInflammation03 medical and health sciencesmedicineAnimalsHumansOmipalisibProtein kinase BPI3K/AKT/mTOR pathwayPharmacologybusiness.industryCUT LIVERmedicine.diseaseMice Inbred C57BLMODEL030104 developmental biologybusinessMATRIXEx vivoBiochemical Pharmacology
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Elafibranor, an Agonist of the Peroxisome Proliferator-Activated Receptor-alpha and -delta, Induces Resolution of Nonalcoholic Steatohepatitis Withou…

2016

International audience; BACKGROUND & AIMS: Elafibranor is an agonist of the peroxisome proliferator-activated receptor-α and peroxisome proliferator-activated receptor-δ. Elafibranor improves insulin sensitivity, glucose homeostasis, and lipid metabolism and reduces inflammation. We assessed the safety and efficacy of elafibranor in an international, randomized, double-blind placebo-controlled trial of patients with nonalcoholic steatohepatitis (NASH).METHODS: Patients with NASH without cirrhosis were randomly assigned to groups given elafibranor 80 mg (n = 93), elafibranor 120 mg (n = 91), or placebo (n = 92) each day for 52 weeks at sites in Europe and the United States. Clinical and …

0301 basic medicineLiver CirrhosisMaleTime FactorsIntention to Treat Analysi[SDV]Life Sciences [q-bio]BiopsyPLACEBO-CONTROLLED TRIALTHERAPYGastroenterologySeverity of Illness IndexChalcone0302 clinical medicineChalconesNon-alcoholic Fatty Liver DiseaseGastrointestinal AgentNonalcoholic fatty liver diseasePropionateMedicine and Health SciencesOdds RatioMedicineGlucose homeostasisVITAMIN-Eeducation.field_of_studyGastrointestinal agentFatty liverRemission InductionGastroenterologyMiddle Aged3. Good healthIntention to Treat AnalysisPPARDEuropeTreatment OutcomeLiverACIDPIOGLITAZONE030211 gastroenterology & hepatologyFemalePPARAHumanSignal TransductionAdultCLINICAL-OUTCOMESmedicine.medical_specialtyLogistic ModelTime FactorLiver CirrhosiPopulationfatty liver; NAFLD; PPARA; PPARD; Adult; Biomarkers; Biopsy; Chalcones; Double-Blind Method; Europe; Female; Gastrointestinal Agents; Humans; Intention to Treat Analysis; Liver; Liver Cirrhosis; Logistic Models; Male; Middle Aged; Non-alcoholic Fatty Liver Disease; Odds Ratio; PPAR alpha; PPAR gamma; Propionates; Remission Induction; Severity of Illness Index; Signal Transduction; Time Factors; Treatment Outcome; United States; GastroenterologyPlacebo03 medical and health sciencesDouble-Blind MethodGastrointestinal AgentsInternal medicineNAFLDHumansPPAR alphaeducationFATTY LIVER-DISEASEfatty liverHepatologybusiness.industryBiomarkerAMERICAN ASSOCIATIONOdds ratiomedicine.diseaseConfidence intervalUnited StatesPPAR gammaRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]030104 developmental biologyEndocrinologyLogistic ModelsHuman medicinePropionatesbusinessBiomarkers
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Refining prediction of survival after TIPS with the novel Freiburg index of post-TIPS survival.

2021

Background & Aims Transjugular intrahepatic portosystemic shunt (TIPS) implantation is an effective and safe treatment for complications of portal hypertension. Survival prediction is important in these patients as they constitute a high-risk population. Therefore, the aim of our study was to develop an alternative prognostic model for accurate survival prediction after planned TIPS implantation. Methods A total of 1,871 patients with de novo TIPS implantation for ascites or secondary prophylaxis of variceal bleeding were recruited retrospectively. The study cohort was divided into a training set (80% of study patients; n = 1,496) and a validation set (20% of study patients; n = 375). Furth…

0301 basic medicineLiver CirrhosisMalemedicine.medical_specialtyCirrhosismedicine.medical_treatmentPopulationClinical Decision-MakingSerum Albumin HumanEsophageal and Gastric Varices03 medical and health sciences0302 clinical medicineRisk FactorsInternal medicineAscitesmedicineSecondary PreventionHumanseducationAgedRetrospective Studieseducation.field_of_studyFramingham Risk ScoreHepatologyProportional hazards modelbusiness.industryAge FactorsAscitesBilirubinMiddle Agedmedicine.diseasePrognosisSurvival Rate030104 developmental biologyTreatment OutcomeResearch DesignCreatinineCohortPortal hypertension030211 gastroenterology & hepatologyFemalemedicine.symptomPortasystemic Shunt Transjugular IntrahepaticbusinessGastrointestinal HemorrhageTransjugular intrahepatic portosystemic shuntJournal of hepatology
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Prevalence and severity of nonalcoholic fatty liver disease by transient elastography: Genetic and metabolic risk factors in a general population.

2017

BACKGROUND & AIMS The worldwide spread of obesity is leading to a dramatic increase in the prevalence of nonalcoholic fatty liver disease (NAFLD) and its complications. We aimed to evaluate both prevalence and factors associated with NAFLD in a general population in a Mediterranean area. METHODS We considered 890 consecutive individuals included in the community-based ABCD (Alimentazione, Benessere Cardiovascolare e Diabete) study (ISRCTN15840340). Controlled attenuation parameter (CAP) and liver stiffness measurement (LSM) were measured with FibroScan. Participants were genotyped for PNPLA3 rs738409 and TM6SF2 rs58542926 variants. RESULTS The prevalence of NAFLD in the cohort was 48%. NAFL…

0301 basic medicineLiver CirrhosisMalesteatosigeneral populationGastroenterologySeverity of Illness Index0302 clinical medicinepatatin like phospholipase domain containing 3FibrosisNon-alcoholic Fatty Liver DiseaseRisk FactorsNonalcoholic fatty liver diseasePrevalenceliver stiffness measurementeducation.field_of_studyMiddle Agedtransient elastographycontrolled attenuation parameterItalyLiverCohortElasticity Imaging Techniquestransmembrane 6 superfamily 2030211 gastroenterology & hepatologyFemalefibrosiAdultmedicine.medical_specialtyPopulationPopulationPolymorphism Single Nucleotide03 medical and health sciencesDiabetes mellitusInternal medicinemedicineDiabetes MellitusHumansObesityeducationstiffneAgedHepatologybusiness.industrynutritional and metabolic diseasesMembrane ProteinsLipasemedicine.diseaseObesitydigestive system diseases030104 developmental biologyLogistic ModelsTransient elastographybusinessTM6SF2Liver international : official journal of the International Association for the Study of the Liver
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PARP inhibition enhances tumor cell-intrinsic immunity in ERCC1-deficient non-small cell lung cancer.

2018

The cyclic GMP-AMP synthase/stimulator of IFN genes (cGAS/STING) pathway detects cytosolic DNA to activate innate immune responses. Poly(ADP-ribose) polymerase inhibitors (PARPi) selectively target cancer cells with DNA repair deficiencies such as those caused by BRCA1 mutations or ERCC1 defects. Using isogenic cell lines and patient-derived samples, we showed that ERCC1-defective non-small cell lung cancer (NSCLC) cells exhibit an enhanced type I IFN transcriptomic signature and that low ERCC1 expression correlates with increased lymphocytic infiltration. We demonstrated that clinical PARPi, including olaparib and rucaparib, have cell-autonomous immunomodulatory properties in ERCC1-defecti…

0301 basic medicineLung NeoplasmsDNA repairPoly (ADP-Ribose) Polymerase-1Triple Negative Breast NeoplasmsPoly(ADP-ribose) Polymerase InhibitorsPoly (ADP-Ribose) Polymerase InhibitorB7-H1 AntigenOlaparib03 medical and health scienceschemistry.chemical_compoundInterferon-gamma0302 clinical medicinePARP1Carcinoma Non-Small-Cell LungHumansRucaparibA549 cellChemistryBRCA1 ProteinMembrane ProteinsGeneral MedicineEndonucleasesIsogenic human disease modelsNucleotidyltransferasesDNA-Binding Proteins030104 developmental biologyA549 Cells030220 oncology & carcinogenesisCancer cellCancer researchFemaleResearch ArticleThe Journal of clinical investigation
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MET-EGFR dimerization in lung adenocarcinoma is dependent on EGFR mtations and altered by MET kinase inhibition

2017

Advanced lung cancer has poor survival with few therapies. EGFR tyrosine kinase inhibitors (TKIs) have high response rates in patients with activating EGFR mutations, but acquired resistance is inevitable. Acquisition of the EGFR T790M mutation causes over 50% of resistance; MET amplification is also common. Preclinical data suggest synergy between MET and EGFR inhibitors. We hypothesized that EGFR-MET dimerization determines response to MET inhibition, depending on EGFR mutation status, independently of MET copy number. We tested this hypothesis by generating isogenic cell lines from NCI-H1975 cells, which co-express L858R and T790M EGFR mutations, namely H1975L858R/T790M (EGFR TKI resista…

0301 basic medicineLung NeoplasmsKinase InhibitorsCancer Treatmentlcsh:MedicinePhysical ChemistryBiochemistryFluorophotometryT790MSpectrum Analysis Techniques0302 clinical medicineFluorescence Resonance Energy TransferMedicine and Health SciencesPhosphorylationEnzyme Inhibitorslcsh:ScienceExtracellular Signal-Regulated MAP KinasesEGFR inhibitorsStainingMice Inbred BALB CMultidisciplinaryFluorescent in Situ HybridizationPhysicsCell StainingProto-Oncogene Proteins c-metPrecipitation TechniquesErbB ReceptorsChemistryOncologySpectrophotometry030220 oncology & carcinogenesisPhysical SciencesErlotinibDimerizationProtein BindingResearch Articlemedicine.drugChemical physicsMice NudeMolecular Probe TechniquesAdenocarcinoma of LungAdenocarcinomaBiologyResearch and Analysis Methods03 medical and health sciencesGefitinibGrowth factor receptorCell Line TumormedicineAnimalsHumansImmunoprecipitationMolecular Biology TechniquesLung cancerProtein Kinase InhibitorsMolecular BiologyCell ProliferationCell growthlcsh:RReproducibility of ResultsBiology and Life SciencesDimers (Chemical physics)medicine.diseaseMolecular biologyIsogenic human disease modelsProbe Hybridizationrespiratory tract diseasesHEK293 Cells030104 developmental biologyChemical PropertiesSpecimen Preparation and TreatmentFocal Adhesion Protein-Tyrosine KinasesMutationEnzymologylcsh:QProtein MultimerizationProto-Oncogene Proteins c-aktCytogenetic TechniquesPLOS ONE
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A molecular hypothesis to explain direct and inverse co-morbidities between Alzheimer's Disease, Glioblastoma and Lung cancer.

2017

Epidemiological studies indicate that patients suffering from Alzheimer’s disease have a lower risk of developing lung cancer, and suggest a higher risk of developing glioblastoma. Here we explore the molecular scenarios that might underlie direct and inverse co-morbidities between these diseases. Transcriptomic meta-analyses reveal significant numbers of genes with inverse patterns of expression in Alzheimer’s disease and lung cancer, and with similar patterns of expression in Alzheimer’s disease and glioblastoma. These observations support the existence of molecular substrates that could at least partially account for these direct and inverse co-morbidity relationships. A functional analy…

0301 basic medicineLung NeoplasmsMolecular biology[SDV]Life Sciences [q-bio]Gene ExpressionDiseaseCàncer--Fisiologia patològicaComorbidityTranscriptomeMedicineDinàmica molecularMultidisciplinaryQLung Cancer:Enginyeria biomèdica [Àrees temàtiques de la UPC]R3. Good healthAlzheimer's disease (AD)MedicineDisease SusceptibilityAlzheimer's diseaseSignal transductionSignal TransductionCentral Nervous System (CNS)ScienceModels BiologicalArticle03 medical and health sciencesImmune systemcáncerAlzheimer DiseaseDementia[CHIM]Chemical SciencesHumansLung cancerbusiness.industryGenetic Variationmedicine.diseaseComorbidityCNS cancerAlzheimer Malaltia d'030104 developmental biologyGliobastomas (GBM)ImmunologyCancer researchDementiabusinessGlioblastomaReactive Oxygen SpeciesNon-small-cell lung cancerBiomarkers
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Comprehensive Analysis of SWI/SNF Inactivation in Lung Adenocarcinoma Cell Models

2020

Simple Summary: Mammalian SWI/SNF complexes regulate gene expression by reorganizing the way DNA is packaged into chromatin. SWI/SNF subunits are recurrently altered in tumors at multiple levels, including DNA mutations as well as alteration of the levels of RNA and protein. Cancer cell lines are often used to study SWI/SNF function, but their patterns of SWI/SNF alterations can be complex. Here, we present a comprehensive characterization of DNA mutations and RNA and protein expression of SWI/SNF members in 38 lung adenocarcinoma (LUAD) cell lines. We show that over 85% of our cell lines harbored at least one alteration in one SWI/SNF subunit. In addition, over 75% of our cell lines lacked…

0301 basic medicineLung adenocarcinomaCancer ResearchcellsCellgenetic processesmacromolecular substancesBiologylcsh:RC254-282Articlelaw.inventionTranscriptome03 medical and health sciences0302 clinical medicinelawmedicineEpigeneticsMulti-omicsSWI/SNF complexepigeneticsCancermulti-omicslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaselung adenocarcinomaSWI/SNFcell models3. Good healthCell biologyChromatinenzymes and coenzymes (carbohydrates)lung cancer030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCell modelSuppressorEpigeneticsbiological phenomena cell phenomena and immunityLung cancerSWI/SNF complex
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Biallelic variants in LARS2 and KARS cause deafness and (ovario)leukodystrophy

2019

Supplemental Digital Content is available in the text.

0301 basic medicineLysine-tRNA LigaseMalePathologyMagnetic Resonance SpectroscopyMedizinmembrane proteins030204 cardiovascular system & hematologyMitochondrionDeafnessmedicine.disease_causeCompound heterozygosityCorrectionsLeukoencephalopathyMyelin0302 clinical medicineCytosolLeukoencephalopathies030212 general & internal medicineOvarian DiseasesTransfer RNA AminoacylationChildZebrafishMUTATIONExome sequencing10012MutationBrainMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]General MedicineMiddle AgedDisorders of movement Donders Center for Medical Neuroscience [Radboudumc 3]Magnetic Resonance ImagingMitochondriaProtein Transportendoplasmic reticulummedicine.anatomical_structureChild PreschoolTransfer RNAComputingMethodologies_DOCUMENTANDTEXTPROCESSING/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_being[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Biological AssayFemaleWRBRare cancers Radboud Institute for Health Sciences [Radboudumc 9]Adultcardiomyopathiesmedicine.medical_specialtyMitochondrial diseaseAminoacylationMuscle disorderBiologyArticleMEDIATES INSERTIONAmino Acyl-tRNA Synthetases03 medical and health sciencesSDG 3 - Good Health and Well-beingmedicineAnimalsPoint MutationHumansAmino Acid SequenceAlleleAllelesCOMPLEXGenetic heterogeneitybusiness.industryArsenite Transporting ATPasesLeukodystrophyGenetic Variation10090Original ArticlesZebrafish Proteinsbiology.organism_classificationDILATED CARDIOMYOPATHYmedicine.diseasezebrafishGENEMolecular biologyDisease Models Animal030104 developmental biologyMembrane protein[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human genetics10084Neurology (clinical)Transfer RNA AminoacylationMEMBRANEbusinessSequence Alignment030217 neurology & neurosurgeryexomeNeurology
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