Search results for " FIBROSIS"

showing 10 items of 490 documents

Encapsulating peritoneal sclerosis: do not be too late for the right diagnosis! Case report and short literature review

2020

Encapsulating peritoneal sclerosis (EPS) is a rare clinical syndrome characterized by an acquired, inflammatory fibrocollagenous membrane encasing the small intestine, resulting in symptoms of bowel obstruction. It is still unclear whether early surgical intervention has an advantage over conservative management, but, in most reviewed case reports, it is preferred to preserve the surgical management in patients not responding to conservative measures, or when bowel ischaemia is occurring. We report a case of a 58-year old patients, affected by chronic renal failure, on treatment with peritoneal dialysis, in which a late diagnosis of encapsulating peritoneal sclerosis was made, and where sur…

MaleLaparotomyPolycystic Kidney DiseasesDelayed DiagnosisPeritoneal FibrosisMiddle AgedConservative TreatmentSettore MED/18 - Chirurgia GeneraleFatal OutcomeEncapsulating peritoneal sclerosis (EPS)HumansKidney Failure ChronicTomography X-Ray ComputedPeritoneal Dialysis
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Anti-inflammatory and anti-fibrotic profile of fish oil emulsions used in parenteral nutrition-associated liver disease.

2014

Home parenteral nutrition (PN) is associated with many complications including severe hepatobiliary dysfunction. Commercial ω-6 fatty acid-soybean based-lipid emulsions in PN may mediate long term PN associate liver disease (PNALD) whereas ω-3-fish oil parenteral emulsions have shown to reverse PNALD in children. However, its clinical effectiveness in adults has been scarcely reported. In this work, we study the role of soybean and fish oil lipid commercial emulsions on inflammatory and profibrotic liver markers in adults with long term PNALD and in in vitro cellular models. Inflammatory and profibrotic markers were measured in serum of ten adults with long term PNALD and in culture superna…

MaleLipopolysaccharideAnti-Inflammatory AgentsCell Culture Techniqueslcsh:MedicinePharmacologySoybean oilChronic Liver DiseaseLiver diseasechemistry.chemical_compoundMedicine and Health Scienceslcsh:ScienceMultidisciplinaryLiver DiseasesFatty liverMiddle AgedFish oilLiver FibrosisFemalemedicine.symptomParenteral Nutrition HomeResearch ArticleAdultFat Emulsions Intravenousfood.ingredientEpithelial-Mesenchymal Transitionmedicine.drug_classImmunologyInflammationGastroenterology and HepatologyAnti-inflammatoryImmunomodulationCicatrixfoodFish OilsFatty Acids Omega-6medicineHumansTriglyceridesAgedNutritionbusiness.industrylcsh:RBiology and Life Sciencesmedicine.diseaseNutritional DiseasesSoybean OilParenteral nutritionchemistryImmunologylcsh:QbusinessPloS one
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VEB-1 in Achromobacter xylosoxidans from Cystic Fibrosis Patient, France

2006

Multidrug-resistant Achromobacter xylosoxidans was recovered from the sputum of a patient with cystic fibrosis. The VEB-1 extended-spectrum β-lactamase was detected on a class 1 integron. This first report of a VEB-1–producing isolate in this population requires further investigation to determine its distribution.

MaleMESH : Molecular Sequence DataintegronMESH: beta-Lactamaseslcsh:MedicineMESH: Base Sequence[ SDV.MP.BAC ] Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyIntegronCystic fibrosisIntegronscystic fibrosisComputingMilieux_MISCELLANEOUSMESH: Microbial Sensitivity Tests0303 health scienceseducation.field_of_studybiologyEscherichia coli ProteinsMESH : beta-LactamasesAchromobacter denitrificansdispatchAchromobacter xylosoxidansMESH: Integrons3. Good healthMESH : Achromobacter denitrificansFrancemedicine.symptomAchromobacter xylosoxidansMESH : IntegronsMESH: Cystic FibrosisAdolescentMESH : MaleMolecular Sequence DataPopulationMicrobial Sensitivity Testsbeta-LactamasesMicrobiologylcsh:Infectious and parasitic diseases03 medical and health sciencesMESH : AdolescentMESH : Cystic FibrosismedicineHumansBase sequencelcsh:RC109-216education030304 developmental biologyMESH: AdolescentMESH: HumansMESH: Molecular Sequence DataBase Sequence030306 microbiologybusiness.industryMESH : Humanslcsh:RExtended-spectrum beta-lactamase VEB-1biology.organism_classificationmedicine.disease[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyMESH: MaleMESH: Achromobacter denitrificansAchromobacter denitrificansbiology.proteinSputumMESH : Base SequenceMESH : Microbial Sensitivity Tests[SDV.MP.BAC] Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologybusinessEmerging Infectious Diseases
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MUC16 Is Overexpressed in Idiopathic Pulmonary Fibrosis and Induces Fibrotic Responses Mediated by Transforming Growth Factor-β1 Canonical Pathway

2021

Several transmembrane mucins have demonstrated that they contribute intracellularly to induce fibrotic processes. The extracellular domain of MUC16 is considered as a biomarker for disease progression and death in IPF patients. However, there is no evidence regarding the signalling capabilities of MUC16 that contribute to IPF development. Here, we demonstrate that MUC16 was overexpressed in the lung tissue of IPF patients (n = 20) compared with healthy subjects (n = 17) and localised in fibroblasts and hyperplastic alveolar type II cells. Repression of MUC16 expression by siRNA-MUC16 transfection inhibited the TGF-β1-induced fibrotic processes such as mesenchymal/ myofibroblast transformati…

MaleMUC16Gene ExpressionIdiopathic pulmonary fibrosis0302 clinical medicineBiology (General)PhosphorylationMyofibroblastsLungSpectroscopytransforming growth factor betabiologyChemistryGeneral MedicineTransfectionMiddle Agedrespiratory systemidiopathic pulmonary fibrosisImmunohistochemistryRespiratory Function TestsComputer Science ApplicationsChemistrymedicine.anatomical_structure030220 oncology & carcinogenesisFemaleDisease SusceptibilityMyofibroblastSignal TransductionQH301-705.5Models BiologicalArticleCatalysisCell LineTransforming Growth Factor beta1Inorganic Chemistry03 medical and health sciencesmedicineHumansPhysical and Theoretical ChemistryFibroblastQD1-999Molecular BiologyAgedCell ProliferationA549 cellOrganic ChemistryMesenchymal stem cellMembrane ProteinsTransforming growth factor betaFibroblastsmedicine.diseaserespiratory tract diseases030228 respiratory systemCA-125 AntigenCase-Control StudiesCancer researchbiology.proteinIdiopathic Pulmonary Fibrosis ; Muc16 ; Transforming Growth Factor BetaBiomarkersTransforming growth factorInternational Journal of Molecular Sciences
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Acceleration of glutathione efflux and inhibition of gamma-glutamyltranspeptidase sensitize metastatic B16 melanoma cells to endothelium-induced cyto…

2005

Highly metastatic B16 melanoma (B16M)-F10 cells, as compared with the low metastatic B16M-F1 line, have higher GSH content and preferentially overexpress BCL-2. In addition to its anti-apoptotic properties, BCL-2 inhibits efflux of GSH from B16M-F10 cells and thereby may facilitate metastatic cell resistance against endothelium-induced oxidative/nitrosative stress. Thus, we investigated in B16M-F10 cells which molecular mechanisms channel GSH release and whether their modulation may influence metastatic activity. GSH efflux was abolished in multidrug resistance protein 1 knock-out (MRP-/-1) B16M-F10 transfected with the Bcl-2 gene or in MRP-/-1 B16M-F10 cells incubated with l-methionine, wh…

MaleMelanoma ExperimentalCystic Fibrosis Transmembrane Conductance RegulatorApoptosisBiochemistryOligodeoxyribonucleotides Antisensechemistry.chemical_compoundMiceCell AdhesionAnimalsEndotheliumNeoplasm MetastasisCytotoxicityCell adhesionMolecular BiologybiologyActivator (genetics)Cell BiologyGlutathioneTransfectiongamma-GlutamyltransferaseMolecular biologyGlutathioneCystic fibrosis transmembrane conductance regulatorMice Inbred C57BLKineticsOxidative StresschemistryProto-Oncogene Proteins c-bcl-2VerapamilApoptosisbiology.proteinEffluxMultidrug Resistance-Associated ProteinsThe Journal of biological chemistry
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Upregulation of activin-B and follistatin in pulmonary fibrosis: a translational study using human biopsies and a specific inhibitor in mouse fibrosi…

2014

Background: Activins are members of the TGF-ß superfamily of growth factors. First, we identified by expression array screening that activin-B and follistatin are upregulated in human idiopathic pulmonary fibrosis (IPF). Next, we wanted to clarify their specific role in lung fibrosis formation. Methods: We used specific antibodies for activin-A and -B subunits and follistatin to measure and localize their levels in idiopathic pulmonary fibrosis and control lung biopsies. To inhibit activin signaling, we used soluble activin type IIB receptor fused to the Fc portion of human IgG1 (sActRIIB-Fc) in two different mouse models of pulmonary fibrosis. Results: Activin-B and follistatin mRNA levels…

MalePathologyFollistatinPulmonary FibrosisPROTEINCell CountQuadriceps MuscleACTIVATIONIdiopathic pulmonary fibrosisMiceBMP-7FibrosisPulmonary fibrosisfollistatinInhibin-beta SubunitsGREMLINImmunity Cellularmedicine.diagnostic_testbiologyactivinsPIRFENIDONEPirfenidonerespiratory systemidiopathic pulmonary fibrosisMouse fibrosis model3. Good healthUp-RegulationActivinsmedicine.anatomical_structureACUTE EXACERBATIONmouse fibrosis modelembryonic structuresGROWTHBronchoalveolar Lavage Fluidhormones hormone substitutes and hormone antagonistsmedicine.drugResearch ArticleSignal TransductionPulmonary and Respiratory MedicineEXPRESSIONmedicine.medical_specialtyendocrine systemRecombinant Fusion ProteinseducationIdiopathic pulmonary fibrosisRespiratory MucosaAlveolar cellsINFLAMMATIONmedicineAnimalsHumansRNA MessengerLungbusiness.industrymedicine.diseaserespiratory tract diseasesMice Inbred C57BLPulmonary AlveoliDisease Models AnimalBronchoalveolar lavageProtein Biosynthesis3121 General medicine internal medicine and other clinical medicinebiology.proteinbusinessFollistatin
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Expanding the clinical spectrum of hereditary fibrosing poikiloderma with tendon contractures, myopathy and pulmonary fibrosis due to FAM111B mutatio…

2015

Background Hereditary Fibrosing Poikiloderma (HFP) with tendon contractures, myopathy and pulmonary fibrosis (POIKTMP [MIM 615704]) is a very recently described entity of syndromic inherited poikiloderma. Previously by using whole exome sequencing in five families, we identified the causative gene, FAM111B (NM_198947.3), the function of which is still unknown. Our objective in this study was to better define the specific features of POIKTMP through a larger series of patients. Methods Clinical and molecular data of two families and eight independent sporadic cases, including six new cases, were collected. Results Key features consist of: (i) early-onset poikiloderma, hypotrichosis and hypoh…

MalePathologyMyopathyPulmonary FibrosisMedicine/Public HealthCell Cycle ProteinsGrowthHypotrichosisContracturesTendons030207 dermatology & venereal diseases0302 clinical medicineFibrosisPulmonary fibrosisSerineGenetics(clinical)Pharmacology (medical)TrypsinExomeChildGenetics (clinical)FAM111BSkinMedicine(all)0303 health sciencesMicroscopyMuscle WeaknessMusclesSkin Diseases GeneticGeneral MedicineMiddle AgedMagnetic Resonance ImagingMuscle atrophy3. Good healthMuscular AtrophyTissuesLiverChild PreschoolFemalemedicine.symptomAdultmedicine.medical_specialtyContractureAdolescentMolecular Sequence DataPoikiloderma03 medical and health sciencesPoikilodermaMuscular DiseasesmedicineHumansAdiposisAmino Acid SequenceCysteineExocrine pancreatic insufficiencyMyopathyMuscle Skeletal030304 developmental biologyMuscle contractureHypohidrosisSclerosisbusiness.industryResearchInfantProteinsmedicine.diseaseFibrosisGenesMutationSkin AbnormalitiesHypotrichosisExocrine Pancreatic Insufficiencybusiness
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TIMP expression in toxic and cholestatic liver injury in rat.

1997

Abstract Background/Aims: Hepatic fibrosis is a dynamic pathological process with a net accumulation of extracellular matrix proteins. Recent evidence suggests that besides their increased synthesis, inhibition of matrix degradation plays a significant role. ECM degradation occurs via metalloproteinases which are inhibited in situ by specific tissue inhibitors of metalloproteinases (TIMPs). The aim of our studies was to determine the expression of TIMPs during toxic liver injury and cholestatic liver injury leading to fibrosis. Methods: We examined the expression of TIMP-1, -2 and -3 in two different rat models for liver injury (intraperitoneal CCl 4 injection and bile duct ligation) by Nor…

MalePathologymedicine.medical_specialtyIn situ hybridizationCholestasis IntrahepaticMatrix metalloproteinaseBiologyRats Sprague-DawleyCholestasisFibrosisInternal medicinemedicineAnimalsNorthern blotIn Situ HybridizationLiver injuryTissue Inhibitor of Metalloproteinase-3Tissue Inhibitor of Metalloproteinase-2Tissue Inhibitor of Metalloproteinase-1HepatologyCarbon Tetrachloride PoisoningAcute-phase proteinTissue Inhibitor of Metalloproteinasesmedicine.diseaseRatsEndocrinologyLiverChemical and Drug Induced Liver InjuryHepatic fibrosisJournal of hepatology
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Transient Elastography-Based Liver Stiffness Age-Dependently Increases in Children

2016

Background and Aims Pediatric use of liver transient elastography (TE) is attractive for its non-invasiveness, but reference values have not been established. We aimed to determine reference values for TE in children. Methods In pediatric patients (1 to 18 years), TE (FibroScan®) with an M probe was used for both liver stiffness measurement (LSM) and measurement of hepatic fat deposition by using a controlled attenuation parameter (CAP). The patients were divided into three relevant age groups: preschoolers (1 to 5 years), elementary school children (6 to 11 years), and adolescents (12 to 18 years). Overweight or obese patients or those with known liver disease, elevated serum liver enzymes…

MalePercentilePhysiologylcsh:MedicineSocial SciencesOverweightAdolescentsPediatricsGastroenterologyLiver disease0302 clinical medicineSociologyReference ValuesRisk FactorsMedicine and Health Sciences030212 general & internal medicinelcsh:ScienceChildSchoolsMultidisciplinaryLiver DiseasesFatty liverLiverPhysiological ParametersChild PreschoolElasticity Imaging TechniquesLiver FibrosisFemale030211 gastroenterology & hepatologymedicine.symptomResearch Articlemedicine.medical_specialtyChildhood ObesityAdolescentGastroenterology and HepatologyChildhood obesityEducation03 medical and health sciencesLiver stiffnessInternal medicinemedicineHumansObesitybusiness.industrylcsh:RBody WeightInfantBiology and Life SciencesEchogenicitymedicine.diseaseFatty LiverAge GroupsPeople and Placeslcsh:QPopulation GroupingsTransient elastographybusinessPLOS ONE
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Vascular effects of sildenafil in patients with pulmonary fibrosis and pulmonary hypertension: an ex vivo/in vitro study

2015

Sildenafil improves the 6-min walking distance in patients with idiopathic pulmonary fibrosis (IPF) and right-sided ventricular systolic dysfunction.We analysed the previously unexplored role of sildenafil on vasoconstriction and remodelling of pulmonary arteries from patients with IPF and pulmonary hypertension (PH) ex vivo. Pulmonary arteries from 18 donors without lung disease, nine IPF, eight PH+IPF and four PH patients were isolated to measure vasodilator and anti-contractile effects of sildenafil in isometric organ bath. Ventilation/perfusion was explored in an animal model of bleomycin lung fibrosis.Sildenafil relaxed serotonin (5-HT) pre-contracted pulmonary arteries in healthy dono…

MalePulmonary FibrosisVasodilator AgentsVasodilation030204 cardiovascular system & hematologyPulmonary Disease Chronic ObstructiveIdiopathic pulmonary fibrosischemistry.chemical_compound0302 clinical medicinePulmonary fibrosisMyofibroblastsLungrespiratory systemExtracellular Matrixmedicine.anatomical_structurecardiovascular systemCardiologymedicine.symptomSignal TransductionPulmonary and Respiratory MedicineSerotoninmedicine.medical_specialtyEndotheliumSildenafilHypertension PulmonaryMyocytes Smooth MusclePulmonary ArterySildenafil CitrateTransforming Growth Factor beta1Bleomycin03 medical and health sciencesmedicine.arteryInternal medicinemedicineAnimalsHumansRats Wistarbusiness.industryFibroblastsmedicine.diseasePulmonary hypertensionRatsrespiratory tract diseasesDisease Models Animal030228 respiratory systemchemistryVasoconstrictionPulmonary arteryEndothelium VascularbusinessVasoconstrictionEuropean Respiratory Journal
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