Search results for "proteinas"

showing 10 items of 416 documents

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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Vasculitic wallenberg syndrome with detection of anti-proteinase 3 antibodies in the cerebrospinal fluid of a patient with severe Wegener's granuloma…

2000

MalePathologymedicine.medical_specialtyMyeloblastinAutoantigensAntibodies Antineutrophil CytoplasmicCerebrospinal fluidProteinase 3MyeloblastinMedicineHumansLungLateral Medullary SyndromeAutoantibodiesTransplantationKidneyLateral medullary syndromeLungmedicine.diagnostic_testbusiness.industrySerine EndopeptidasesAutoantibodyGranulomatosis with PolyangiitisMagnetic resonance imagingMiddle Agedmedicine.diseaseMagnetic Resonance Imagingmedicine.anatomical_structureNephrologybusinessTomography X-Ray ComputedNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
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Matrix metalloproteinases production in malignant pleural effusions after talc pleurodesis

2003

SUMMARY In this study we have evaluated the modifications of matrix metalloproteinases (MMPs) in malignant pleural fluids taken from patients suffering from lung cancer and treated with intrapleural talc instillation to induce pleurodesis. Furthermore, we have analysed the variations of some inflammatory mediators (C-reactive protein, α-1 antitrypsin) and of a protein (plasminogen) involved in MMP activation. In all patients the clinical improvement after talc pleurodesis was followed by a reduction in MMP-1, TIMP-1, C-reactive protein, α-1 antitrypsin and plasminogen activity. Furthermore, MMP-9 levels were variable; in fact, in some patients they were high at the beginning of treatment, i…

MalePathologymedicine.medical_specialtyPleural effusionmedicine.medical_treatmentImmunologyMatrix metalloproteinaseTalcStatistics NonparametricClinical StudiesHumansImmunology and AllergyMedicineLung cancerPleurodesisAgedTissue Inhibitor of Metalloproteinase-1business.industryTalc pleurodesisA proteinPlasminogenMiddle Agedmedicine.diseaseMatrix MetalloproteinasesPleural Effusion MalignantC-Reactive ProteinMatrix Metalloproteinase 9Talcalpha 1-AntitrypsinImmunologyPleural fluidFemaleMatrix Metalloproteinase 1businessPleurodesismedicine.drugClinical and Experimental Immunology
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Aprotinin inhibits leukocyte–endothelial cell interactions after hemorrhage and reperfusion

2003

Background. The serine protease inhibitor aprotinin has been successfully used to reduce blood loss in patients undergoing cardiac operations. We studied aprotinin for its ability to modulate leukocyte– endothelial cell interactions after ischemia and reperfusion. Methods. The effects of aprotinin on leukocyte– endothelial cell interactions were observed by intravital microscopy in the rat mesenteric microcirculation and immunohistochemical analysis. The inflammatory cascade (leukocyte rolling, firm adherence, and transmigration) was studied after thrombin stimulation and after hemorrhage and reperfusion. Results. Intravenous bolus administration of aprotinin treatment (20,000 U/kg) signifi…

MalePulmonary and Respiratory MedicineSerine Proteinase InhibitorsEndotheliumHemorrhageInflammationLeukocyte RollingCell CommunicationPharmacologyMicrocirculationRats Sprague-DawleyAprotininThrombinLeukocytesmedicineAnimalsMesenteryAprotininbusiness.industryMicrocirculationThrombinImmunohistochemistryRatsEndothelial stem cellP-Selectinmedicine.anatomical_structureReperfusionImmunologySurgeryEndothelium Vascularmedicine.symptomCardiology and Cardiovascular Medicinebusinesshormones hormone substitutes and hormone antagonistsIntravital microscopymedicine.drugThe Annals of Thoracic Surgery
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Induction of RAGE Shedding by Activation of G Protein-Coupled Receptors

2011

The multiligand Receptor for Advanced Glycation End products (RAGE) is involved in various pathophysiological processes, including diabetic inflammatory conditions and Alzheimers disease. Full-length RAGE, a cell surface-located type I membrane protein, can proteolytically be converted by metalloproteinases ADAM10 and MMP9 into a soluble RAGE form. Moreover, administration of recombinant soluble RAGE suppresses activation of cell surface-located RAGE by trapping RAGE ligands. Therefore stimulation of RAGE shedding might have a therapeutic value regarding inflammatory diseases. We aimed to investigate whether RAGE shedding is inducible via ligand-induced activation of G protein-coupled recep…

MaleReceptors Vasopressinendocrine system diseasesReceptor for Advanced Glycation End Productslcsh:MedicineHydroxamic Acids570 Life sciencesRAGE (receptor)Adenylyl cyclaseADAM10 ProteinMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundMolecular Cell BiologyNeurobiology of Disease and RegenerationSignaling in Cellular ProcessesMembrane Receptor SignalingReceptors Immunologiclcsh:ScienceReceptorLungCellular Stress ResponsesCalcium signalingMultidisciplinaryKinaseDipeptidesHormone Receptor SignalingCell biologyMatrix Metalloproteinase 9NeurologyReceptors OxytocinGene Knockdown Techniquescardiovascular systemMatrix Metalloproteinase 2Pituitary Adenylate Cyclase-Activating PolypeptideMedicineRNA InterferenceAdenylyl CyclasesResearch ArticleSignal Transduction570 Biowissenschaftenmedicine.medical_specialtyMAP Kinase Signaling SystemADAM17 ProteinBiologyAlzheimer DiseaseCa2+/calmodulin-dependent protein kinaseInternal medicinemedicineAnimalsHumansProtease InhibitorsCalcium Signalingcardiovascular diseasesBiologyG protein-coupled receptorlcsh:RHEK 293 cellsMembrane Proteinsnutritional and metabolic diseasesCyclic AMP-Dependent Protein KinasesADAM ProteinsG-Protein SignalingHEK293 CellsEndocrinologychemistryProteolysisDementialcsh:QAmyloid Precursor Protein SecretasesMolecular Neurosciencehuman activitiesReceptors Pituitary Adenylate Cyclase-Activating Polypeptide Type INeurosciencePLoS ONE
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Two‐dimensional analysis of myocardial protein expression following myocardial ischemia and reperfusion in rabbits

2002

Myocardial ischemia and reperfusion injury (MI/R) can be related to leukocyte activation with subsequent release of cytokines and oxygen derived free radicals. Activation of the complement system has been implicated in the pathogenesis of myocardial ischemia and reperfusion injury. Inflammatory injury will subsequently result in cellular activation and protein synthesis. In the present study we analyzed the myocardial protein expression and its pattern following myocardial ischemia and reperfusion, with and without complement inhibition with the synthetic serine protease inhibitor Futhan/nafamstat mesilate (FUT-175) known to inhibit classical and alternative complement pathway in a rabbit m…

MaleSerine Proteinase InhibitorsNecrosisProteomeNeutrophilsMyocardial IschemiaIschemiaMyocardial Reperfusion InjuryPharmacologyGuanidinesBiochemistrySuperoxide dismutaseNecrosisRandom AllocationComplement inhibitormedicineAnimalsElectrophoresis Gel Two-DimensionalCreatine KinaseMolecular BiologybiologySuperoxide DismutaseChemistryGene Expression ProfilingMyocardiumHemodynamicsProteinsalpha-Crystallin B Chainmedicine.diseaseBenzamidinesComplement systemBiochemistrybiology.proteinAlternative complement pathwayCreatine kinaseRabbitsmedicine.symptomReperfusion injuryPROTEOMICS
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Expression of MMP-2 and MMP-9 in odontogenic myxoma in a child: report of a clinical case

2011

Odontogenic myxoma (OM) is a benign, locally invasive, non-metastasizing neoplasm of the jaw bones. Despite the benign nature of these lesions, there is a high rate of recurrence and the current recommended therapy, depending on the size and behaviour of the lesion, can vary from curettage with peripheral ostectomy, segmental resection up to radical resections for more aggressive lesions. OM is a rare tumour which occurs predominantly in the third decade of life and it is rare in children. Matrix metalloproteinases (MMPs) are a family of extracellular endopeptidases responsible for the degradation and remodelling of extracellular matrix, they are known to be involved in the progression and …

MaleSettore BIO/17 - IstologiaPathologymedicine.medical_specialtymedicine.medical_treatmentOdontogenic TumorsBiologyInferior alveolar nerveMatrix metalloproteinaseOdontogenic myxomaLesionExtracellular matrixSettore MED/28 - Malattie OdontostomatologichemedicineHumansChildGeneral DentistryDNA PrimersBase SequenceReverse Transcriptase Polymerase Chain Reactionmedicine.diseaseCurettageMatrix Metalloproteinase 9ImmunohistochemistryMatrix Metalloproteinase 2medicine.symptomSegmental resectionMyxomaOdontogenic myxoma Child MMP-2 MMP-9 it
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MMP-2, MMP-9, and iNOS Expression in Human Dental Pulp Subjected to Orthodontic Traction

2009

Abstract Objective: To test the hypothesis that some metalloproteinases (MMP-2, MMP-9) and inducible nitric oxide synthetase (iNOS) enzymes in dental pulp samples do not vary when subjected to orthodontic treatment. Materials and Methods: Human dental pulps were taken from male and female patients (N=10; age 10–14 years). A straight wire technique was used with nickel-titanium or steel archwires. The increase of pressure applied on teeth was gradual. Five patients were subjected to premolar extractions after 14 months of treatment and one after 24 months. Samples were Bouin-fixed, paraffin-embedded, and afterwards processed for immunohistochemistry using anti-MMP-2, anti-MMP-9, and anti-iNO…

MaleSettore BIO/17 - IstologiaTime FactorsNitric oxide synthetaseAdolescentTooth Movement TechniquesNitric Oxide Synthase Type IIDentistryOrthodonticsMalocclusion Angle Class IIMatrix metalloproteinaseNickelFemale patientOrthodontic WiresPressurePremolarHumansMedicineBicuspidChildTitaniumOdontoblastsMMP-2Orthodontic wirebusiness.industrymedicine.diseaseImmunohistochemistryBiomechanical PhenomenaDental pulpiNOSmedicine.anatomical_structureMatrix Metalloproteinase 9SteelMatrix Metalloproteinase 2ImmunohistochemistryFemaleStress MechanicalTreatment timeMalocclusionMMP-9businessImmunohistochemistry Dental pulp MMP-2 MMP-9 iNOS.Dental AlloysFollow-Up StudiesThe Angle Orthodontist
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Heme oxygenase-1 regulates the progression of K/BxN serum transfer arthritis.

2012

Background Heme oxygenase-1 (HO-1) is induced in many cell types as a defense mechanism against stress. We have investigated the possible role of endogenous HO-1 in the effector phase of arthritis using the K/BxN serum transfer model of arthritis in HO-1 heterozygous and homozygous knock-out mice. Methodology/Principal Findings Arthritis was induced in C57/Black-6 xFVB (HO-1+/+, HO-1+/− and HO-1−/−) mice by intraperitoneal injection of 150 µl serum from arthritic K/BxN mice at days 0 and 2. Blood was collected and animals were sacrificed at day 10. Histological analysis was performed in ankle sections. The levels of inflammatory mediators were measured in serum and paw homogenates by enzyme…

MaleTime FactorsAnatomy and PhysiologyMouseNon-Clinical MedicineArthritislcsh:MedicineEndogenyBiochemistryAntioxidantsMicechemistry.chemical_compoundDrug Discoverylcsh:ScienceMusculoskeletal SystemHemeRegulation of gene expressionMultidisciplinaryEffectorSystems BiologyAnimal ModelsEnzymesDisease ProgressionMedicineMatrix Metalloproteinase 3Inflammation Mediatorsmedicine.symptomResearch ArticleCell typeOsteocalcinRheumatoid ArthritisInflammationModel OrganismsRheumatologymedicineAnimalsBiologyBlood CellsRANK Ligandlcsh:Rmedicine.diseaseArthritis ExperimentalMolecular biologyMice Inbred C57BLHeme oxygenaseDisease Models AnimalGene Expression RegulationchemistryImmunologylcsh:QAnkle JointHeme Oxygenase-1PLoS ONE
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Effects of small interfering RNAs targeting fascin on human esophageal squamous cell carcinoma cell lines

2010

Abstract Background Fascin induces membrane protrusions and cell motility. Fascin overexpression was associated with poor prognosis, and its downregulation reduces cell motility and invasiveness in esophageal squamous cell carcinoma (ESCC). Using a stable knockdown cell line, we revealed the effect of fascin on cell growth, cell adhesion and tumor formation. Methods We examined whether fascin is a potential target in ESCC using in vitro and in vivo studies utilizing a specific siRNA. We established a stable transfectant with downregulated fascin from KYSE170 cell line. Results The fascin downregulated cell lines showed a slower growth pattern by 40.3% (p In vivo, the tumor size was signific…

MaleTime FactorsHistologyEsophageal NeoplasmsMice NudeApoptosismacromolecular substancesCysteine Proteinase InhibitorsBiologyTransfectionAmino Acid Chloromethyl KetonesPathology and Forensic MedicineExtracellular matrixMiceDownregulation and upregulationCell Line TumorCell Adhesionlcsh:PathologyAnimalsHumansRNA Small InterferingCell adhesionCell ProliferationFascinMice Inbred BALB CCell growthResearchMicrofilament ProteinsGeneral MedicineTransfectionCaspase InhibitorsXenograft Model Antitumor AssaysTumor BurdenCell biologyCell cultureApoptosisCaspasesCarcinoma Squamous Cellbiology.proteinRNA InterferenceCollagenCarrier Proteinslcsh:RB1-214Diagnostic Pathology
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