Search results for "reverse transcriptase"

showing 10 items of 715 documents

The effect of the pro-inflammatory cytokine tumor necrosis factor-alpha on human joint capsule myofibroblasts.

2009

Introduction Previous studies have shown that the number of myoblastically differentiated fibroblasts known as myofibroblasts (MFs) is significantly increased in stiff joint capsules, indicating their crucial role in the pathogenesis of post-traumatic joint stiffness. Although the mode of MFs' function has been well defined for different diseases associated with tissue fibrosis, the underlying mechanisms of their regulation in the pathogenesis of post-traumatic joint capsule contracture are largely unknown. Methods In this study, we examined the impact of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-α) on cellular functions of human joint capsule MFs. MFs were challenged w…

MalePathologymedicine.medical_treatmentFluorescent Antibody TechniqueGene ExpressionDinoprostExtracellular matrixPathogenesisElbow JointImmunology and AllergyCells CulturedReverse Transcriptase Polymerase Chain ReactionAntibodies MonoclonalMiddle AgedImmunohistochemistryExtracellular MatrixCytokinemedicine.anatomical_structureAntirheumatic AgentsCytokinesTumor necrosis factor alphaFemaleHip Jointmedicine.symptomInflammation MediatorsMyofibroblastmusculoskeletal diseasesmedicine.medical_specialtyanimal structuresContractureDiclofenacImmunologyBlotting Westernmacromolecular substancesBiologyCollagen Type IDinoprostoneRheumatologyJoint capsuleResearch articlemedicineHumansAgedCell ProliferationCyclooxygenase 2 InhibitorsTumor Necrosis Factor-alphaProstaglandins FFibroblastsActinsInfliximabCyclooxygenase 2Joint stiffnessContractureJoint CapsuleArthritis researchtherapy
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First Evidence for a Crosstalk Between Mitochondrial and NADPH Oxidase-Derived Reactive Oxygen Species in Nitroglycerin-Triggered Vascular Dysfunction

2008

Chronic nitroglycerin treatment results in development of nitrate tolerance associated with endothelial dysfunction (ED). We sought to clarify how mitochondria- and NADPH oxidase (Nox)-derived reactive oxygen species (ROS) contribute to nitrate tolerance and nitroglycerin-induced ED. Nitrate tolerance was induced by nitroglycerin infusion in male Wistar rats (100 microg/h/4 day) and in C57/Bl6, p47(phox/) and gp91(phox/) mice (50 microg/h/4 day). Protein and mRNA expression of Nox subunits were unaltered by chronic nitroglycerin treatment. Oxidative stress was determined in vascular rings and mitochondrial fractions of nitroglycerin-treated animals by L-012 enhanced chemiluminescence, revea…

MalePhysiologyVasodilator AgentsClinical BiochemistryMitochondrionPharmacologymedicine.disease_causeBiochemistryMitochondria HeartMiceNitroglycerinchemistry.chemical_compoundEthidiumAortaChromatography High Pressure LiquidHeart metabolismGeneral Environmental Sciencechemistry.chemical_classificationNADPH oxidasebiologyReverse Transcriptase Polymerase Chain ReactionReactive Nitrogen SpeciesBiochemistryCyclosporinecardiovascular systemcirculatory and respiratory physiologyBlotting WesternIn Vitro TechniquesTransfectionCell LineRotenonemedicineAnimalsHumansRNA MessengerRats WistarMolecular BiologyReactive oxygen speciesNADPH OxidasesCell BiologyRotenoneRatsMice Inbred C57BLchemistryMitochondrial permeability transition poreVasoconstrictionApocyninbiology.proteinGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidative stressAntioxidants & Redox Signaling
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Downregulation of nNOS and synthesis of PGs associated with endotoxin-induced delay in gastric emptying

2002

A single intraperitoneal injection of endotoxin (40 μg/kg) significantly delayed gastric emptying of a solid nutrient meal. Blockade of nitric oxide synthase (NOS) with 30 mg/kg ip N G-nitro-l-arginine methyl ester or 20 mg/kg ip 7-nitroindazole [neuronal NOS (nNOS) inhibitor] significantly delayed gastric emptying in control animals but failed to modify gastric emptying in endotoxin-treated rats. Administration of 2.5, 5, and 10 mg/kg ip N 6-iminoethyl-l-lysine [inducible NOS (iNOS) inhibitor] had no effect in either experimental group. Indomethacin (5 mg/kg sc), NS-398 (cyclooxygenase-2 inhibitor; 10 mg/kg ip), and dexamethasone (10 mg/kg sc) but not quinacrine (20 mg/kg ip) significantl…

MalePhysiologymedicine.medical_treatmentIndomethacinNitric Oxide Synthase Type IINitric Oxide Synthase Type IprostaglandinsRats Sprague-Dawleychemistry.chemical_compoundPyloric AntrumEnzyme InhibitorsAntrumSulfonamidesArachidonic AcidbiologyReverse Transcriptase Polymerase Chain ReactionStomachdigestive oral and skin physiologyGastroenterologyNitric oxide synthasemedicine.anatomical_structureNG-Nitroarginine Methyl EsterQuinacrinenutrient mealsantrum. pylorusmedicine.medical_specialtyIndazolesIntraperitoneal injectionNitric OxidePhospholipases ANitric oxidenitric oxidePhysiology (medical)Internal medicinemedicineAnimalsCyclooxygenase InhibitorsRNA MessengerNitrobenzenesHepatologyGastric emptyingPylorusdigestive system diseasesRatsEndotoxinsEndocrinologyPyloric AntrumchemistryGastric EmptyingFoodbiology.proteinProstaglandinsNitric Oxide Synthase
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Embryonic stem cell-related miRNAs are involved in differentiation of pluripotent cells originating from the germ line.

2010

Cells originating from the germ cell lineage retain the remarkable property under special culture conditions to give rise to cells with embryonic stem cell (ESC) properties, such as the multipotent adult germline stem cells (maGSCs) derived from adult mouse testis. To get an insight into the mechanisms that control pluripotency and differentiation in these cells, we studied how differences observed during in vitro differentiation between ESCs and maGSCs are associated with differences at the level of microRNAs (miRNAs). In this work, we provide for a first time a connection between germ cell origin of maGSCs and their specific miRNA expression profile. We found that maGSCs express higher le…

MalePluripotent Stem CellsEmbryologyEmbryonic Germ CellsAdult Germline Stem CellsCellular differentiationBiology03 medical and health sciencesMice0302 clinical medicineGeneticsmedicineAnimalsCell LineageComputer SimulationInduced pluripotent stem cellMolecular BiologyEmbryonic Stem Cells030304 developmental biologyGenetics0303 health sciencesReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingMultipotent Stem CellsObstetrics and GynecologyCell DifferentiationCell BiologyEmbryonic stem cellCell biologyMicroRNAsmedicine.anatomical_structureGerm CellsReproductive MedicineGerm line developmentStem cell030217 neurology & neurosurgeryGerm cellBiomarkersDevelopmental BiologyMolecular human reproduction
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A novel two base pair deletion in the factor V gene associated with severe factor V deficiency

2001

We studied a family in which the proband, a 13-year-old boy, had unmeasurable plasma levels of coagulation factor V antigen and activity. Clinical symptoms were severe, with several episodes of haemorrhages in the mucosal tracts (gastrointestinal, nose and urinary) and recurrent haemarthroses that caused permanent arthropathy. Sequence analysis of the factor V gene demonstrated the presence of a novel 2 base pair (bp) homozygous deletion in exon 13 at positions 2833-2834. This mutation, present in the heterozygous state in the asymptomatic mother and absent in the healthy brother, introduced a frameshift and a premature stop at codon 900. This would predict the synthesis of a truncated fact…

MaleProbandFactor V DeficiencyAdolescentMutantBiologymedicine.disease_causeFrameshift mutationExonmedicineHumansRNA MessengerBase PairingGeneGeneticsMutationReverse Transcriptase Polymerase Chain ReactionHomozygoteFactor VFactor VSequence Analysis DNAHematologyMolecular biologybiology.proteinBlood Coagulation TestsFactor V DeficiencyGene DeletionBritish Journal of Haematology
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Nitric Oxide Mediates Natural Polyphenol-induced Bcl-2 Down-regulation and Activation of Cell Death in Metastatic B16 Melanoma

2007

Intravenous administration to mice of trans-pterostilbene (t-PTER; 3,5-dimethoxy-4'-hydroxystilbene) and quercetin (QUER; 3,3',4',5,6-pentahydroxyflavone), two structurally related and naturally occurring small polyphenols, inhibits metastatic growth of highly malignant B16 melanoma F10 (B16M-F10) cells. t-PTER and QUER inhibit bcl-2 expression in metastatic cells, which sensitizes them to vascular endothelium-induced cytotoxicity. However, the molecular mechanism(s) linking polyphenol signaling and bcl-2 expression are unknown. NO is a potential bioregulator of apoptosis with controversial effects on Bcl-2 regulation. Polyphenols may affect NO generation. Short-term exposure (60 min/day) t…

MaleProgrammed cell deathCeramideEndotheliumDown-RegulationBiologyNitric OxideBiochemistryMicechemistry.chemical_compoundPhenolsCell Line TumorCell AdhesionmedicineAnimalsRNA MessengerNeoplasm MetastasisCytotoxicityMelanomaMolecular BiologyNitritesFlavonoidsNitratesCell DeathReverse Transcriptase Polymerase Chain ReactionPolyphenolsHydrogen PeroxideCell BiologyGenes bcl-2Cell biologyMice Inbred C57BLEndothelial stem cellmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2Mitochondrial permeability transition porechemistryCell cultureApoptosisMitochondrial MembranesCancer researchEndothelium VascularJournal of Biological Chemistry
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Phosphodiesterase 4 inhibition decreases MUC5AC expression induced by epidermal growth factor in human airway epithelial cells

2005

Background: A common pathological feature of chronic inflammatory airway diseases such as asthma and chronic obstructive pulmonary disease (COPD) is mucus hypersecretion. MUC5AC is the predominant mucin gene expressed in healthy airways and is increased in asthmatic and COPD patients. Recent clinical trials indicate that phosphodiesterase type 4 (PDE4) inhibitors may have therapeutic value for COPD and asthma. However, their direct effects on mucin expression have been scarcely investigated. Methods: MUC5AC mRNA and protein expression were examined in cultured human airway epithelial cells (A549) and in human isolated bronchial tissue stimulated with epidermal growth factor (EGF; 25 ng/ml).…

MalePulmonary and Respiratory Medicinemedicine.medical_specialtyBlotting WesternBronchiEnzyme-Linked Immunosorbent AssayRespiratory MucosaMucin 5ACp38 Mitogen-Activated Protein KinasesWestern blotEpidermal growth factorInternal medicineGene expressionCyclic AMPmedicineHumansRNA MessengerPhosphotyrosineCells CulturedRoflumilastRolipramAgedA549 cellEpidermal Growth Factormedicine.diagnostic_testReverse Transcriptase Polymerase Chain Reactionbusiness.industryCilomilastMucinMucinsEpithelial CellsMiddle Agedrespiratory systemMolecular biologyRecombinant ProteinsCyclic Nucleotide Phosphodiesterases Type 4respiratory tract diseasesEndocrinology3'5'-Cyclic-AMP PhosphodiesterasesAirway BiologyFemalebusinessmedicine.drugThorax
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Docosahexaenoic acid reduces suppressive and migratory functions of CD4CD25 regulatory T-cells

2009

Immunological tolerance is one of the fundamental aspects of the immune system. The CD4(+)CD25(+) regulatory T (Treg) cells have emerged as key players in the development of tolerance to self and foreign antigens. However, little is known about the endogenous factors and mechanisms controlling their suppressive capacity on immune response. In this study, we observed that docosahexaenoic acid (DHA), an n-3 polyunsaturated fatty acid, diminished, in a dose-dependent manner, the capacity of Treg cells to inhibit the CD4(+)CD25(-) effector T-cell proliferation. DHA not only reduced the migration of Treg cells toward chemokines but also downregulated the mRNA expression of CCR-4 and CXCR-4 in Tr…

MaleReceptors CXCR4Chemokineextracellular signal-regulated kinase 1/2Receptors CCR4Docosahexaenoic Acidschemical and pharmacologic phenomenaQD415-436T-Lymphocytes RegulatoryBiochemistryMicehistone desacetylase 7EndocrinologyImmune systemAntigenAntigens CDCell MovementTransforming Growth Factor betaAnimalsCTLA-4 AntigenRNA MessengerIL-2 receptorCells CulturedCell ProliferationDose-Response Relationship DrugbiologySmad7Reverse Transcriptase Polymerase Chain ReactionInterleukin-2 Receptor alpha SubunitFOXP3Forkhead Transcription Factorshemic and immune systemsCell BiologyTransforming growth factor betaInterleukin-10Cell biologyMice Inbred C57BLInterleukin 10Docosahexaenoic acidImmunologybiology.proteinResearch ArticleJournal of Lipid Research
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Dicer and drosha expression and response to bevacizumab-based therapy in advanced colorectal cancer patients.

2013

PURPOSE: The miRNA-regulating enzymes Dicer and Drosha exhibit aberrant expression in several cancer types. Dicer and Drosha play a crucial role during the angiogenetic process in vitro and, for Dicer, in vivo. We aimed to investigate the potential role of Dicer and Drosha in predicting response to Bevacizumab-based therapy in advanced colorectal cancer (CRC) patients. METHODS: Dicer and Drosha mRNA levels were analysed in formalin-fixed paraffin-embedded specimens from patients affected by advanced CRC treated with or without Bevacizumab-containing regimens (n=116 and n=50, respectively) and from patients with diverticulosis as control group (n=20). The experimental data were obtained usin…

MaleRibonuclease IIICancer ResearchSettore MED/06 - Oncologia Medicagenetic processesAngiogenesis InhibitorsKaplan-Meier EstimateDEAD-box RNA HelicasesangiogenesisIntestinal MucosaOligonucleotide Array Sequence AnalysisAged 80 and overReverse Transcriptase Polymerase Chain Reactionfood and beveragesMiddle AgedPrognosisImmunohistochemistryCRCBevacizumabGene Expression Regulation NeoplasticqPCRTreatment OutcomeOncologyMonoclonalImmunohistochemistryFemaleColorectal Neoplasmsmedicine.drugAdultBevacizumabBiologyAntibodies Monoclonal HumanizedDroshaYoung AdultSDG 3 - Good Health and Well-beingmicroRNAmedicineHumansDroshamiRNAAgedGene Expression ProfilingfungiCancermedicine.diseaseGene expression profilingenzymes and coenzymes (carbohydrates)miRNA; angiogenesisMultivariate AnalysisCancer researchbiology.proteinBevacizumab; CRC; Dicer; Drosha; miRNAs; qPCRDicerDicer
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Convergent sets of data from in vivo and in vitro methods point to an active role of Hsp60 in chronic obstructive pulmonary disease pathogenesis.

2011

BackgroundIt is increasingly clear that some heat shock proteins (Hsps) play a role in inflammation. Here, we report results showing participation of Hsp60 in the pathogenesis of chronic obstructive pulmonary diseases (COPD), as indicated by data from both in vivo and in vitro analyses.Methods and resultsBronchial biopsies from patients with stable COPD, smoker controls with normal lung function, and non-smoker controls were studied. We quantified by immunohistochemistry levels of Hsp10, Hsp27, Hsp40, Hsp60, Hsp70, Hsp90, and HSF-1, along with levels of inflammatory markers. Hsp10, Hsp40, and Hsp60 were increased during progression of disease. We found also a positive correlation between th…

MaleSTRESSPulmonologyChronic Obstructive Pulmonary DiseasesNeutrophilsBiopsyGene ExpressionCD8-Positive T-Lymphocytesmedicine.disease_causeBiochemistryEpitheliumPulmonary function testingPathogenesisACTIVATIONPulmonary Disease Chronic ObstructiveMolecular Cell BiologyLungCOPDMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionCOPD Hsp60QRCOPD heat shock proteins inflammationMiddle AgedImmunohistochemistrymedicine.anatomical_structureEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISMedicineFemalemedicine.symptomInflammation MediatorsSPINAL-CORDResearch ArticleEXPRESSIONanimal structuresCOPD; heat shock proteins; inflammationScienceImmunologyMolecular Sequence DataInflammationBronchichemical and pharmacologic phenomenaHEAT-SHOCK-PROTEIN EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS ACUTE LUNG INJURY SPINAL-CORD CELL-DEATH KAPPA-B HEAT-SHOCK-PROTEIN-60 STRESS EXPRESSION ACTIVATIONKAPPA-BBiologyHEAT-SHOCK-PROTEINMicrobiologycomplex mixturesCell LineACUTE LUNG INJURYMolecular GeneticsIn vivoStress PhysiologicalHeat shock proteinmedicineGeneticsHumansCOPDRNA MessengerBiologyAgedLungMucous MembraneBase SequenceSettore BIO/16 - Anatomia UmanaMacrophagesfungiImmunityTranscription Factor RelAProteinsComputational BiologyChaperonin 60medicine.diseaseChaperone Proteinsrespiratory tract diseasesGene Expression RegulationCELL-DEATHHEAT-SHOCK-PROTEIN-60inflammationImmunologyheat shock proteinsClinical ImmunologyOxidative stressBiomarkers
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