Search results for "Fibrosis"

showing 10 items of 901 documents

Genome-wide association study of non-alcoholic fatty liver and steatohepatitis in a histologically characterised cohort☆

2020

Background & Aims: Genetic factors associated with nonalcoholic fatty liver disease (NAFLD) remain incompletely understood. To date, most genome-wide association studies (GWASs) have adopted radiologically assessed hepatic triglyceride content as the reference phenotype and so cannot address steatohepatitis or fibrosis. We describe a GWAS encompassing the full spectrum of histologically characterised NAFLD. Methods: The GWAS involved 1,483 European NAFLD cases and 17,781 genetically matched controls. A replication cohort of 559 NAFLD cases and 945 controls was genotyped to confirm signals showing genome-wide or close to genome-wide significance. Results: Case-control analysis identified…

0301 basic medicineMaleCirrhosis17-Hydroxysteroid DehydrogenasesFibrosiVARIANTLOCIPROGRESSIONGenome-wide association studyDiseaseBioinformaticsDISEASECohort Studies0302 clinical medicineNon-alcoholic Fatty Liver DiseaseRisk FactorsGWASINCREASED RISKCONFERS SUSCEPTIBILITYeducation.field_of_studyFatty liverNASHMiddle Aged3. Good healthNAFLD; NASH; Fibrosis; GWAS; PNPLA3; TM6SF2; GCKR; HSD17B13; SNPPhenotypeLiver030211 gastroenterology & hepatologyFemaleLife Sciences & BiomedicineGCKRAdultPopulationSNP610 Medicine & healthGastroenterology and HepatologyPolymorphism Single NucleotideTM6SF2HSD17B1303 medical and health sciencesNAFLDmedicineGastroenterologiHumansGenetic Predisposition to DiseaseeducationPNPLA3Adaptor Proteins Signal TransducingScience & TechnologyGastroenterology & HepatologyHepatologybusiness.industrynutritional and metabolic diseasesMembrane ProteinsLipasemedicine.diseaseFibrosisPOLYMORPHISMLEPTIN RECEPTOR GENE030104 developmental biology3121 General medicine internal medicine and other clinical medicineCase-Control StudiesHuman medicineSteatosisSteatohepatitisbusinessTM6SF2Genome-Wide Association StudyJournal of Hepatology
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Genetic Variation in HSD17B13 Reduces the Risk of Developing Cirrhosis and Hepatocellular Carcinoma in Alcohol Misusers.

2020

Background and aims Carriage of rs738409:G in patatin-like phospholipase domain containing 3 (PNPLA3) is associated with an increased risk for developing alcohol-related cirrhosis and hepatocellular carcinoma (HCC). Recently, rs72613567:TA in hydroxysteroid 17-beta dehydrogenase 13 (HSD17B13) was shown to be associated with a reduced risk for developing alcohol-related liver disease and to attenuate the risk associated with carriage of PNPLA3 rs738409:G. This study explores the risk associations between these two genetic variants and the development of alcohol-related cirrhosis and HCC. Approach and results Variants in HSD17B13 and PNPLA3 were genotyped in 6,171 participants, including 1,03…

0301 basic medicineMaleCirrhosis17-Hydroxysteroid DehydrogenasesVARIANTPROGRESSIONGastroenterologyCohort StudiesLiver disease0302 clinical medicineSNP RS738409G ALLELEDEPENDENCELiver Cirrhosis Alcoholic600 Technology610 Medicine & healthAged 80 and overeducation.field_of_studyFramingham Risk ScoreLiver NeoplasmsASSOCIATIONlipotoxicityMiddle AgedAlcoholism1101 Medical Biochemistry and Metabolomics1107 ImmunologyHepatocellular carcinomaadiponutrin030211 gastroenterology & hepatologyFemalecandidate genesLife Sciences & Biomedicinemedicine.medical_specialtyCarcinoma HepatocellularPopulation610 Medicine & healthLower riskRisk Assessment03 medical and health sciencesLIVER-DISEASEInternal medicinemedicinegenetic risk associationHumansAdiponutrineducationPNPLA3METAANALYSISAgedDISEASE-ASSOCIATED MORTALITYScience & TechnologyHepatologyGastroenterology & Hepatologybusiness.industryfibrosisGenetic Variation1103 Clinical SciencesOdds ratiomedicine.disease030104 developmental biologyhost geneticsbusinessgenetic susceptibility
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Antibiotic resistance and population structure of cystic fibrosis Pseudomonas aeruginosa isolates from a Spanish multi-centre study

2017

The first Spanish multi-centre study on the microbiology of cystic fibrosis (CF) was conducted from 2013 to 2014. The study involved 24 CF units from 17 hospitals, and recruited 341 patients. The aim of this study was to characterise Pseudomonas aeruginosa isolates, 79 of which were recovered from 75 (22%) patients. The study determined the population structure, antibiotic susceptibility profile and genetic background of the strains. Fifty-five percent of the isolates were multi-drug-resistant, and 16% were extensively drug-resistant. Defective mutS and mutL genes were observed in mutator isolates (15.2%). Considerable genetic diversity was observed by pulsed-field gel electrophoresis (70 p…

0301 basic medicineMaleCystic FibrosisAntibiotic resistanceArray tubeMulti-locus sequence typing (MLST)medicine.disease_causeGenotypePharmacology (medical)ChildGeneticseducation.field_of_studyMolecular EpidemiologyVirulencePseucforrumus aeruginosaGeneral MedicineMiddle AgedMutS DNA Mismatch-Binding ProteinElectrophoresis Gel Pulsed-FieldInfectious DiseasesChild PreschoolPseudomonas aeruginosaFemalemedicine.drugMicrobiology (medical)AdultAdolescentGenotype030106 microbiologyPopulationVirulenceBiologyCystic fibrosisMicrobiology03 medical and health sciencesYoung AdultAntibiotic resistanceDrug Resistance BacterialmedicineHumansPseudomonas InfectionsTypingeducationGenetic diversityPseudomonas aeruginosaGenetic VariationMutL ProteinsSpainColistinMultilocus Sequence Typing
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Plasmacytoid dendritic cells promote systemic sclerosis with a key role for TLR8

2018

Systemic sclerosis (SSc) is a multisystem life-threatening fibrosing disorder that lacks effective treatment. The link between the inflammation observed in organs such as the skin and profibrotic mechanisms is not well understood. The plasmacytoid dendritic cell (pDC) is a key cell type mediating Toll-like receptor (TLR)-induced inflammation in autoimmune disease patients, including lupus and skin diseases with interface dermatitis. However, the role of pDCs in fibrosis is less clear. We show that pDCs infiltrate the skin of SSc patients and are chronically activated, leading to secretion of interferon-α (IFN-α) and CXCL4, which are both hallmarks of the disease. We demonstrate that the s…

0301 basic medicineMaleInflammationPlasmacytoid dendritic cellPlatelet Factor 4SclerodermaArticlePathogenesis03 medical and health sciencesBleomycinMice0302 clinical medicineFibrosismedicineAnimalsHumansSkin030203 arthritis & rheumatologyAutoimmune diseaseSystemic lupus erythematosusScleroderma Systemicintegumentary systembusiness.industryMedicine (all)Interferon-alphahemic and immune systemsGeneral MedicineTLR7Dendritic CellsMiddle Agedmedicine.diseaseFibrosisDisease Models Animal030104 developmental biologyToll-Like Receptor 7Toll-Like Receptor 8ImmunologyFemalemedicine.symptombusinessSignal Transduction
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Combined effects of the PNPLA3 rs738409, TM6SF2 rs58542926, and MBOAT7 rs641738 variants on NAFLD severity: a multicenter biopsy-based study.

2016

The PNPLA3 p.I148M, TM6SF2 p.E167K, and MBOAT7 rs641738 variants represent genetic risk factors for nonalcoholic fatty liver disease (NAFLD). Here we investigate if these polymorphisms modulate both steatosis and fibrosis in patients with NAFLD. We recruited 515 patients with NAFLD (age 16–88 years, 280 female patients). Liver biopsies were performed in 320 patients. PCR-based assays were used to genotype the PNPLA3, TM6SF2, and MBOAT7 variants. Carriers of the PNPLA3 and TM6SF2 risk alleles showed increased serum aspartate aminotransferase and alanine transaminase activities (P 0.05). The MBOAT7 variant was solely associated with increased fibrosis (P = 0.046). In the multivariate model, v…

0301 basic medicineMalePathologyBiopsyBiochemistryGastroenterologySeverity of Illness Index0302 clinical medicineEndocrinologyFibrosisNon-alcoholic Fatty Liver DiseaseGenotypeNonalcoholic fatty liver diseaseAged 80 and overeducation.field_of_studybiologyFatty liverMiddle AgedLiver030211 gastroenterology & hepatologyFemaleAdultmedicine.medical_specialtyAdolescentGenotypePolymorphism Single Nucleotide03 medical and health sciencesYoung AdultInternal medicinemedicineHumansAdiponutrinGenetic Predisposition to DiseaseeducationAllelesGenetic Association StudiesAgedbusiness.industryMembrane ProteinsCell BiologyLipasemedicine.diseaseFibrosisFatty Liver030104 developmental biologyAlanine transaminasebiology.proteinSteatosisbusinessPatient-Oriented and Epidemiological ResearchAcyltransferasesTM6SF2Journal of lipid research
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Evidence of Absorptive Function in vivo in a Neo-Formed Bio-Artificial Intestinal Segment Using a Rodent Model.

2015

A promising therapeutic approach for intestinal failure consists in elongating the intestine with a bio-engineered segment of neo-formed autologous intestine. Using an acellular biologic scaffold (ABS), we, and others, have previously developed an autologous bio-artificial intestinal segment (BIS) that is morphologically similar to normal bowel in rodents. This neo-formed BIS is constructed with the intervention of naïve stem cells that repopulate the scaffold in vivo, and over a period of time, are transformed in different cell populations typical of normal intestinal mucosa. However, no studies are available to demonstrate that such BIS possesses functional absorptive characteristics nece…

0301 basic medicineMalePathologymedicine.medical_specialtyCell typeLumen (anatomy)Bio-artificial intestineBio-engineered intestineIntestinal absorption03 medical and health sciences0302 clinical medicineIntestinal mucosaIn vivoIntestine SmallmedicineAnimalsIntestinal MucosabiologyBioartificial OrgansTissue EngineeringTissue ScaffoldsIn vivo absorptionGastroenterologyCystic fibrosis transmembrane conductance regulatorRatsFunctional analysis of bio-artificial intestine030104 developmental biologyIntestinal Absorptionbiology.proteinUltrastructure030211 gastroenterology & hepatologySurgeryStem cellJournal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
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Blocking CD248 molecules in perivascular stromal cells of patients with systemic sclerosis strongly inhibits their differentiation toward myofibrobla…

2018

Abstract Background Fibrosis may be considered the hallmark of systemic sclerosis (SSc), the end stage triggered by different pathological events. Transforming growth factor-β (TGF-β) and platelet-derived growth factor BB (PDGF-BB) are profibrotic molecules modulating myofibroblast differentiation and proliferation, respectively. There is evidence linking CD248 with these two molecules, both highly expressed in patients with SSc, and suggesting that CD248 may be a therapeutic target for several diseases. The aim of this work was to evaluate the expression of CD248 in SSc skin and its ability to modulate SSc fibrotic process. Methods After ethical approval was obtained, skin biopsies were co…

0301 basic medicineMalelcsh:Diseases of the musculoskeletal systemProton Pump InhibitorFibrosiCellular differentiationmedicine.medical_treatmentSystemic sclerosiFibrosisImmunology and AllergyMedicineMyofibroblastsskin and connective tissue diseasesCells CulturedSkinintegumentary systemCell DifferentiationMiddle AgedMesenchymal Stem CellBenzamidesSystemic sclerosisFemaleMyofibroblastResearch ArticleHumanAdultStromal cellImmunology03 medical and health sciencesYoung AdultRheumatologyBenzamideAntigens CDAntigens NeoplasmHumansGene silencingCell ProliferationMyofibroblastScleroderma Systemicbusiness.industryGrowth factorMesenchymal stem cellStromal CellMesenchymal Stem CellsProton Pump Inhibitorsmedicine.diseaseFibrosisCD248Settore MED/16 - Reumatologia030104 developmental biologyCancer researchStromal Cellslcsh:RC925-935CD248; Fibrosis; Systemic sclerosis; Rheumatology; Immunology and Allergy; ImmunologybusinessTransforming growth factor
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Short-term Changes in Gal 3 Circulating Levels After Acute Myocardial Infarction.

2016

Background and Aims Galectin 3 (Gal 3) is a β-galactoside-binding lectin known to play a part in inflammation, adverse remodeling and fibrosis. Gal 3 seems to be linked to atherogenesis and Coronary Artery Disease (CAD), but less is known about the relationship between Gal 3 and acute myocardial infarction (AMI). The aim of the present study is to assess circulating levels of Gal 3 after AMI and to evaluate short-term changes of the biomarker within 5 days from the acute event. Methods Two hundred fifteen confirmed AMI patients (125 STEMI, M/F = 2.8; mean age: 65.4 ± 13.8 years) were enrolled in the present study; two blood samples were collected from each patient: first, within 1 h from ad…

0301 basic medicineMalemedicine.medical_specialtyTime FactorsGalectin 3Myocardial InfarctionInflammationCoronary Artery Disease030204 cardiovascular system & hematologyAMICoronary artery disease03 medical and health sciences0302 clinical medicineFibrosisInternal medicineMedicineHumansCADcardiovascular diseasesMyocardial infarctionPlaqueAgedInflammationbusiness.industryMedicine (all)Mean ageGeneral MedicineMiddle Agedmedicine.disease030104 developmental biologyGalectin-3ImmunologyCardiologyBiomarker (medicine)Femalemedicine.symptombusinessBiomarkersArchives of medical research
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Rescuing the CFTR protein function: Introducing 1,3,4-oxadiazoles as translational readthrough inducing drugs.

2018

Nonsense mutations in the CFTR gene prematurely terminate translation of the CFTR mRNA leading to the production of a truncated protein that lacks normal function causing a more severe form of the cystic fibrosis (CF) disease. About 10% of patients affected by CF show a nonsense mutation. A potential treatment of this alteration is to promote translational readthrough of premature termination codons (PTCs) by Translational Readthrough Inducing Drugs (TRIDs) such as PTC124. In this context we aimed to compare the activity of PTC124 with analogues differing in the heteroatoms position in the central heterocyclic core. By a validated protocol consisting of computational screening, synthesis an…

0301 basic medicineModels MolecularCell SurvivalNonsense mutationCystic Fibrosis Transmembrane Conductance RegulatorSettore BIO/11 - Biologia MolecolareContext (language use)OxadiazoleSettore BIO/09 - FisiologiaCystic fibrosis03 medical and health sciencesStructure-Activity Relationship0302 clinical medicineDrug DiscoverymedicineHumansRNA MessengerGenetic disorderPharmacologyMessenger RNAOxadiazolesNonsense mutationDose-Response Relationship DrugMolecular StructureChemistryDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryTranslational readthroughPremature termination codonTranslation (biology)Settore CHIM/06 - Chimica OrganicaGeneral Medicinemedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaSmall moleculeCell biologySettore BIO/18 - Genetica030104 developmental biologyBiological targetCystic fibrosi030220 oncology & carcinogenesisHeLa CellsEuropean journal of medicinal chemistry
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Caffeine boosts Ataluren's readthrough activity

2019

Abstract The readthrough of nonsense mutations by small molecules like Ataluren is considered a novel therapeutic approach to overcome the gene defect in several genetic diseases as cystic fibrosis (CF). This pharmacological approach suppresses translation termination at premature termination codons (PTCs readthrough) thus restoring the expression of a functional protein. However, readthrough might be limited by the nonsense-mediated mRNA decay (NMD), a cell process that reduces the amount/level of PTCs containing mRNAs. Here we investigate the combined action of Ataluren and caffeine to enhance the readthrough of PTCs. IB3.1 CF cells with a nonsense mutation were treated with caffeine to a…

0301 basic medicineMolecular biologymedia_common.quotation_subjectCellNonsenseNonsense mutationMRNA DecaySettore BIO/11 - Biologia MolecolareBiochemistryCystic fibrosisArticleCystic fibrosisCFTR gene03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCaffeinemedicinelcsh:Social sciences (General)Settore BIO/06 - Anatomia Comparata E Citologialcsh:Science (General)media_commonMessenger RNAMultidisciplinaryNonsense mutationNonsense mutationsPTC readthroughAtaluren/PTC124Settore CHIM/06 - Chimica Organicamedicine.diseaseCell biologyAtalurenSettore BIO/18 - Genetica030104 developmental biologymedicine.anatomical_structurechemistryCystic fibrosilcsh:H1-99Caffeine030217 neurology & neurosurgerylcsh:Q1-390Heliyon
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