Search results for "Fibrosis"

showing 10 items of 901 documents

Extraction socket healing in rats treated with bisphosphonate: Animal model for bisphosphonate related osteonecrosis of jaws in multiple myeloma pati…

2010

Aim: The aim of this study is to replicate both clinical and histological presentation of bisphosphonate induced osteonecrosis of the jaws (BONJ) in an animal model of the disease state. Successful recapitulation of a BONJlike indication in an animal model will be useful for studying pathogenesis, as well as prevention and treatment strategies for BONJ. Materials and Methods: Eighty (80) rats were prospectively and randomly divided into two groups; control group(40) and study group(40). All animals in study group, injected with a dose of 1 mg/kg dexamethasone (DX) subcutaneously on day 7, 14, or 21; and 1, 2, or 3 doses of 7.5 ?g/kg zoledronic acid (ZA) subcutaneously administered to coinci…

MaleMolarmedicine.medical_specialtymedicine.medical_treatmentFibrosismedicineAnimalsHumansRats WistarTooth SocketGeneral DentistryMultiple myelomaDexamethasoneDental alveolusWound HealingDiphosphonatesbusiness.industryBisphosphonate:CIENCIAS MÉDICAS [UNESCO]medicine.diseaseRatsSurgeryDisease Models AnimalZoledronic acidOtorhinolaryngologyUNESCO::CIENCIAS MÉDICASTooth ExtractionPopulation studyBisphosphonate-Associated Osteonecrosis of the JawSurgeryMultiple Myelomabusinessmedicine.drugMedicina Oral Patología Oral y Cirugia Bucal
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Phase ia/ii, two-arm, open-label, dose-escalation study of oral panobinostat administered via two dosing schedules in patients with advanced hematolo…

2013

Panobinostat is a potent oral pandeacetylase inhibitor that leads to acetylation of intracellular proteins, inhibits cellular proliferation and induces apoptosis in leukemic cell lines. A phase Ia/II study was designed to determine the maximum-tolerated dose (MTD) of daily panobinostat, administered on two schedules: three times a week every week or every other week on a 28-day treatment cycle in patients with advanced hematologic malignancies. The criteria for hematologic dose-limiting toxicities differed between patients with indications associated with severe cytopenias at baseline (leukemia and myeloid disorders) and those less commonly associated with baseline cytopenias (lymphoma and …

MaleOncologyCancer ResearchIndolesMyeloidhodgkin lymphomahydroxamic acidAdministration Oralresponse criteriaPharmacologyHydroxamic Acidst-cell lymphomaHistoneschemistry.chemical_compoundhemic and lymphatic diseasesAged 80 and overHematologyMiddle AgedLeukemiaTreatment Outcomemedicine.anatomical_structuremyelomaOncologyvorinostatHematologic NeoplasmsFemaleAdultmedicine.medical_specialtypanobinostatrefractory multiple-myelomaMaximum Tolerated DoseAntineoplastic AgentsmyelofibrosisNeutropeniahistone deacetylase inhibitorsmyelodysplastic disordersDrug Administration ScheduleYoung AdultInternal medicinePanobinostatmedicineHumansIn patientAdverse effectMyelofibrosisAgedNeoplasm Staginginternational-working-groupacetylationbusiness.industrymedicine.diseaseLymphomachemistryhistone deacetylasehypoxia-inducible factor-1-alphalbh589business
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Disseminated tuberculosis in a patient treated with a JAK2 selective inhibitor: a case report

2012

Abstract Background Primary myelofibrosis is a myeloproliferative disorder characterized by bone marrow fibrosis, abnormal cytokine expression, splenomegaly and anemia. The activation of JAK2 and the increased levels of circulating proinflammatory cytokines seem to play an important role in the pathogenesis of myelofibrosis. Novel therapeutic agents targeting JAKs have been developed for the treatment of myeloproliferative disorders. Ruxolitinib (INCB018424) is the most recent among them. Case presentation To our knowledge, there is no evidence from clinical trials of an increased risk of tuberculosis during treatment with JAK inhibitors. Here we describe the first case of tuberculosis in a…

MaleOncologymedicine.medical_specialtyRuxolitinibTuberculosisSettore MED/17 - Malattie InfettiveAnemiaAntitubercular AgentsMyelofibrosislcsh:MedicineCase ReportGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineMyeloproliferative DisordersInternal medicineNitrilesmedicineHumansTuberculosisMyelofibrosislcsh:Science (General)lcsh:QH301-705.5Medicine(all)Janus kinase 2biologyLatent tuberculosisBiochemistry Genetics and Molecular Biology(all)business.industryTuberculosis Myelofibrosis Ruxolitiniblcsh:RGeneral MedicineJanus Kinase 2medicine.diseasePyrimidinesRuxolitiniblcsh:Biology (General)Primary MyelofibrosisImmunologybiology.proteinPyrazolesbusinessmedicine.druglcsh:Q1-390BMC Research Notes
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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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Vascular damage and lack of angiogenesis in systemic sclerosis skin

2003

The aim of this study was to analyse microvascular damage and compensatory angiogenesis in skin from patients with systemic sclerosis (SSc) compared with systemic lupus erythematosus (SLE), Raynaud's phenomenon (RP) and healthy controls. Immunohistochemistry was used for skin biopsies (9 SSc, 10 SLE, 9 RP and 12 healthy controls) using von Willebrand factor and beta3 integrin subunit specific antibodies, TechMate immunostaining robot and biotin-streptavidin protocol. In the early stages of SSc, vWF was found in the perivascular space and interstitial matrix in papillary but not in the reticular dermis, in particular around small oedematous blood vessels infiltrated by mononuclear cells. The…

MalePathologymedicine.medical_specialtyAngiogenesisNeovascularization PhysiologicConnective tissueRisk AssessmentSeverity of Illness IndexPathogenesis03 medical and health sciences0302 clinical medicineRheumatologyInterstitial matrixVon Willebrand factorReference ValuesFibrosisvon Willebrand FactormedicineHumansLupus Erythematosus SystemicPerivascular spaceskin and connective tissue diseases030304 developmental biology030203 arthritis & rheumatology0303 health sciencesScleroderma Systemicintegumentary systembiologybusiness.industryBiopsy NeedleRaynaud DiseaseGeneral MedicinePrognosismedicine.diseaseImmunohistochemistry3. Good healthDermal papillaemedicine.anatomical_structureCase-Control Studiesbiology.proteinFemaleEndothelium VascularbusinessClinical Rheumatology
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Expression of LFA-1 (CD11a/CD18) and ICAM-1 (CD54) in an animal model of renal interstitial fibrosis induced by unilateral ureteral obstruction

2000

Unilateral ureteral obstruction (UUO) has been used as an experimental model to induce tubulointerstitial damage and interstitial fibrosis. UUO is characterized by cellular proliferation, accumulation of inflammatory cells, and subsequent replacement of renal parenchyma by fibrous tissue. The influx of inflammatory cells into the renal interstitium is mediated by adhesion molecules. In this study, the development of fibrosis in the UUO model of the rat was examined and its relation to the time course of LFA-1 and ICAM-1 expression was assessed by immunohistochemistry. An increase in interstitial connective tissue was detected on day 10 after UUO, with a maximum on day 35. After unilateral u…

MalePathologymedicine.medical_specialtyConnective tissueCD18Kidneyurologic and male genital diseasesToxicologyPathology and Forensic MedicineRats Sprague-DawleyFibrosisAnimalsMedicineLigationHydronephrosisKidneyurogenital systembusiness.industryCell BiologyGeneral MedicineIntercellular Adhesion Molecule-1medicine.diseaseFibrosisLymphocyte Function-Associated Antigen-1female genital diseases and pregnancy complicationsRatsDisease Models Animalmedicine.anatomical_structureCD18 AntigensNephritis InterstitialImmunohistochemistryUreterbusinessNephritisUreteral ObstructionKidney diseaseExperimental and Toxicologic Pathology
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Neutral pH and low–glucose degradation product dialysis fluids induce major early alterations of the peritoneal membrane in children on peritoneal di…

2018

WOS: 000439138700024 PubMed ID: 29776755 The effect of peritoneal dialysates with low-glucose degradation products on peritoneal membrane morphology is largely unknown, with functional relevancy predominantly derived from experimental studies. To investigate this, we performed automated quantitative histomorphometry and molecular analyses on 256 standardized peritoneal and 172 omental specimens from 56 children with normal renal function, 90 children with end-stage kidney disease at time of catheter insertion, and 82 children undergoing peritoneal dialysis using dialysates with low-glucose degradation products. Follow-up biopsies were obtained from 24 children after a median peritoneal dial…

MalePathologymedicine.medical_specialtyEpithelial-Mesenchymal TransitionAdolescentmedicine.medical_treatmentBiopsy030232 urology & nephrologyMedizinPeritonitis030204 cardiovascular system & hematologyPeritonitisperitoneal membranePeritoneal dialysis03 medical and health sciences0302 clinical medicinePeritoneumFibrosisDialysis SolutionsmedicineLymphatic vesselHumansChildDialysisCatheter insertionChemistryInfantHydrogen-Ion Concentrationmedicine.diseaseFibrosismedicine.anatomical_structureGlucoseTreatment Outcomeperitoneal dialysisNephrologyCase-Control StudiesChild PreschoolKidney Failure ChronicFemalePeritoneumchronic kidney diseaseKidney disease
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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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M2 Polarized Macrophages and Giant Cells Contribute to Myofibrosis in Neuromuscular Sarcoidosis

2011

The etiopathogenesis of sarcoidosis, a systemic granulomatous disease, still remains obscure. A multitude of organs have been described to be affected in systemic sarcoidosis. Skeletal muscles may also be affected, leading to myalgia and weakness. A workup of the specific immune response with emphasis on the macrophage response is provided herein. Affected muscle tissue from seven patients with systemic sarcoidosis was analyzed and compared with that from seven patients with other myopathies containing macrophagocytic infiltration. Monocytes/macrophages and giant cells in granulomas of muscle tissue from patients with sarcoidosis show a status of alternative activation (M2) based on their e…

MalePathologymedicine.medical_specialtySystemic diseaseSarcoidosismedicine.medical_treatmentBiologyGiant CellsMonocytesPathology and Forensic MedicineTh2 CellsImmune systemmedicineHumansMacrophageRNA MessengerMuscle SkeletalAgedGranulomaMacrophagesCCL18Cell PolarityEpithelial CellsRegular ArticleNeuromuscular DiseasesMacrophage ActivationMiddle Agedmedicine.diseaseAcquired immune systemFibrosisPhenotypeCytokineGene Expression RegulationGiant cellChemokines CCGranulomaImmunologyCytokinesFemaleThe American Journal of Pathology
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