Search results for "derived"

showing 10 items of 452 documents

Sustained complete hematologic remission after administration of the tyrosine kinase inhibitor imatinib mesylate in a patient with refractory, second…

2002

Abstract Imatinib mesylate, a tyrosine kinase inhibitor targeting bcr-abl, platelet-derived growth factor receptor (PDGF-R), and c-Kit, effectively induces hematologic and cytogenetic remissions in bcr-abl+ chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL) with only mild to moderate side effects. Here, we describe the successful treatment of a 64-year-old man with c-Kit+ secondary acute myeloid leukemia (AML) refractory to standard chemotherapy. Upon 2 weeks of imatinib mesylate administration, the patient achieved a complete hematologic remission in peripheral blood. In addition, complete clearance of leukemic blasts in bone marrow and a significant cytogenetic response…

MaleMyeloidmedicine.drug_classmedicine.medical_treatmentImmunologyAntineoplastic AgentsBiochemistryTyrosine-kinase inhibitorPiperazinesBone MarrowRecurrencehemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsmedicineSecondary Acute Myeloid LeukemiaHumansReceptors Platelet-Derived Growth FactorEnzyme InhibitorsneoplasmsSalvage TherapyChemotherapyAnemia Refractory with Excess of Blastsbusiness.industryAnemia RefractoryDaunorubicinRemission InductionCytarabineMyeloid leukemiaCell BiologyHematologyExonsMiddle Agedmedicine.diseaseNeoplasm ProteinsLeukemiaLeukemia Myeloid AcuteProto-Oncogene Proteins c-kitmedicine.anatomical_structureImatinib mesylatePyrimidinesDrug Resistance NeoplasmImmunologyBenzamidesCancer researchDisease ProgressionImatinib MesylateNeoplastic Stem CellsBone marrowbusinessBlood
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Gene Expression Profiling of Facilitated L-LTP in VP16-CREB Mice Reveals that BDNF Is Critical for the Maintenance of LTP and Its Synaptic Capture

2011

Expression of VP16-CREB, a constitutively active form of CREB, in hippocampal neurons of the CA1 region lowers the threshold for eliciting the late, persistent phase of long-term potentiation (L-LTP) in the Schaffer collateral pathway. This VP16-CREB-mediated L-LTP differs from the conventional late phase of LTP in not being dependent on new transcription. This finding suggests that in the transgenic mice the mRNA transcript(s) encoding the protein(s) necessary for this form of L-LTP might already be present in CA1 neurons in the basal condition. We used high-density oligonucleotide arrays to identify the mRNAs differentially expressed in the hippocampus of transgenic and wild-type mice. We…

MalePatch-Clamp TechniquesTime FactorsTransgeneNeuroscience(all)Long-Term PotentiationNerve Tissue ProteinsDynorphinHippocampal formationCREBHippocampusSynaptic TransmissionMiceNeurotrophic factorsMHC class ImedicineAnimalsRNA MessengerIn Situ HybridizationMice KnockoutNeuronsNeuronal PlasticitybiologyReverse Transcriptase Polymerase Chain ReactionBrain-Derived Neurotrophic FactorGene Expression Profilingmusculoskeletal neural and ocular physiologyGeneral NeuroscienceExcitatory Postsynaptic PotentialsHerpes Simplex Virus Protein Vmw65Long-term potentiationExonsCREB-Binding ProteinMolecular biologyCell biologymedicine.anatomical_structurenervous systemSchaffer collateralSynapsesbiology.proteinFemaleNeuron
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BLBP-expression in astrocytes during experimental demyelination and in human multiple sclerosis lesions

2011

Several lines of evidence indicate that remyelination represents one of the most effective mechanisms to achieve axonal protection. For reasons that are not yet understood, this process is often incomplete or fails in multiple sclerosis (MS). Activated astrocytes appear to be able to boost or inhibit endogenous repair processes. A better understanding of remyelination in MS and possible reasons for its failure is needed. Using the well-established toxic demyelination cuprizone model, we created lesions with either robust or impaired endogenous remyelination capacity. Lesions were analyzed for mRNA expression levels by Affymetrix GeneChip® arrays. One finding was the predominance of immune a…

MalePathologyPlatelet-derived growth factormedicine.medical_treatmentCell CountBehavioral Neurosciencechemistry.chemical_compoundMice0302 clinical medicineFluorescent Antibody Technique IndirectOligonucleotide Array Sequence AnalysisPlatelet-Derived Growth Factor0303 health sciencesGlial fibrillary acidic proteinbiologyExperimental autoimmune encephalomyelitisAstrocytomaMiddle AgedImmunohistochemistrymedicine.anatomical_structureFemaleFibroblast Growth Factor 2Fatty Acid-Binding Protein 7Adultmedicine.medical_specialtyEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisImmunologyBlotting WesternNerve Tissue ProteinsFatty Acid-Binding ProteinsReal-Time Polymerase Chain ReactionTransfection03 medical and health sciencesCuprizoneCell Line TumorGlial Fibrillary Acidic ProteinmedicineAnimalsHumansRNA MessengerRemyelination030304 developmental biologyAgedEndocrine and Autonomic SystemsMultiple sclerosisGrowth factorTumor Suppressor Proteinsmedicine.diseaseOligodendrocyteMice Inbred C57BLchemistryAstrocytesbiology.proteinOsteopontinCarrier Proteins030217 neurology & neurosurgeryDemyelinating Diseases
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Time-course of GDNF and its receptor expression after brain injury in the rat

2008

Abstract The aim of the present work was to perform, by in situ hybridization, a time-course analysis of the glial cell line-derived neurotrophic factor (GDNF) and its receptor mRNA expression in two models of brain injury in the rat: (a) excitotoxic lesion by ibotenic acid injection in the hippocampal formation; (b) mechanical lesion by needle insertion through the cerebral cortex including the white matter of the corpus callosum. The time-course analysis, ranging from 6 h to 8 days, showed that the GDNF and its receptor (RET, GFRα-1 and GFRα-2) mRNA expressions were differentially up-regulated in both models of lesion. This in vivo regulation of the GDNF and its receptor mRNA expression i…

MalePathologymedicine.medical_specialtyGlial Cell Line-Derived Neurotrophic Factor ReceptorsTime FactorsReceptor expressionCentral nervous systemBiologyHippocampal formationSettore BIO/09 - FisiologiaLesionchemistry.chemical_compoundNeurotrophic factorsGlial cell line-derived neurotrophic factormedicineAnimalsGlial Cell Line-Derived Neurotrophic FactorRNA MessengerRats WistarIbotenic AcidGeneral NeuroscienceGDNF RET GFRalfa-1 GFRalfa-2 Brain injury In situ hybridizationRatsmedicine.anatomical_structureGene Expression Regulationnervous systemchemistryCerebral cortexBrain Injuriesbiology.proteinAutoradiographymedicine.symptomIbotenic acidNeuroscience Letters
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Exogenous t-PA Administration Increases Hippocampal Mature BDNF Levels. Plasmin- or NMDA-Dependent Mechanism?

2014

International audience; Brain-derived neurotrophic factor (BDNF) through TrkB activation is central for brain functioning. Since the demonstration that plasmin is able to process pro-BDNF to mature BDNF and that these two forms have opposite effects on neuronal survival and plasticity, a particular attention has been paid to the link between tissue plasminogen activator (tPA)/plasmin system and BDNF metabolism. However, t-PA via its action on different N-methyl-D-aspartate (NMDA) receptor subunits is also considered as a neuromodulator of glutamatergic transmission. In this context, the aim of our study was to investigate the effect of recombinant (r)t-PA administration on brain BDNF metabo…

MalePlasminlcsh:MedicineTropomyosin receptor kinase BBiochemistryMechanical Treatment of SpecimensHippocampusTissue plasminogen activator[SCCO]Cognitive scienceCell SignalingNeurotrophic factorsNeurobiology of Disease and RegenerationMedicine and Health SciencesMembrane Receptor SignalingFibrinolysinBRAINlcsh:ScienceMultidisciplinaryNeuromodulationNeurotransmitter Receptor SignalingNeurochemistryLong-term potentiationNeurotransmittersDENDRITIC GROWTHNEURONAL DEATHRECEPTORSElectroporationNeurologySpecimen DisruptionTranexamic AcidTissue Plasminogen ActivatorACTIVATORTPANMDA receptor[ SCCO ] Cognitive scienceLONG-TERM POTENTIATIONResearch ArticleSignal Transductionmedicine.drugmedicine.medical_specialtyN-MethylaspartateResearch and Analysis MethodsNeuropharmacologyDevelopmental NeuroscienceInternal medicinemedicineAnimalsReceptor trkBProtein PrecursorsRats WistarSPATIAL MEMORYBrain-derived neurotrophic factorBrain-Derived Neurotrophic Factorlcsh:RBiology and Life SciencesCell BiologySYNAPTIC-PLASTICITYRetractionEndocrinologynervous systemSpecimen Preparation and TreatmentSynaptic plasticitylcsh:QMolecular NeuroscienceDizocilpine MaleateNEUROTROPHIC FACTORNeuroscienceSynaptic PlasticityPLoS ONE
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Protein expression profiling suggests relevance of noncanonical pathways in isolated pulmonary embolism

2019

Abstract Patients with isolated pulmonary embolism (PE) have a distinct clinical profile from those with deep vein thrombosis (DVT)-associated PE, with more pulmonary conditions and atherosclerosis. These findings suggest a distinct molecular pathophysiology and the potential involvement of alternative pathways in isolated PE. To test this hypothesis, data from 532 individuals from the Genotyping and Molecular Phenotyping of Venous ThromboEmbolism Project, a multicenter prospective cohort study with extensive biobanking, were analyzed. Targeted, high-throughput proteomics, machine learning, and bioinformatic methods were applied to contrast the acute-phase plasma proteomes of isolated PE pa…

MaleProteomeDatasets as TopicComorbidity030204 cardiovascular system & hematologyProteomicsBioinformaticsBiochemistryThrombosis and HemostasisMachine LearningPathogenesis0302 clinical medicineProtein-Arginine Deiminase Type 2Prospective StudiesProtein Interaction MapsProspective cohort study0303 health scienceseducation.field_of_studyVenous ThromboembolismHematologyMiddle AgedThrombosisPhenotypePulmonary embolismProteomeN-AcetylgalactosaminyltransferasesFemaleAdultQuantitative Trait LociImmunologyPopulationInterferon-gamma03 medical and health sciencesInterleukin-15 Receptor alpha SubunitmedicineHumansGlial Cell Line-Derived Neurotrophic FactoreducationAged030304 developmental biologybusiness.industryPulmonary SurfactantsCell BiologyAtherosclerosismedicine.diseaseOxidative StressGene Expression RegulationPulmonary EmbolismTranscriptomebusinessAcute-Phase ProteinsFollow-Up StudiesBlood
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Brain-Derived Neurotrophic Factor But Not Forced Arm Use Improves Long-Term Outcome After Photothrombotic Stroke and Transiently Upregulates Binding …

2008

Background and Purpose— Both application of neurotrophic factors like brain-derived neurotrophic factor (BDNF) and constraint-induced movement therapy like forced arm use have been shown to potentially improve outcome after stroke. The aim of the present study was to check whether postischemic long-term outcome correlates to specific modifications in the abundance of various neurotransmitter receptors. Methods— Adult male Wistar rats were subjected to photothrombotic ischemia and assigned to various treatment groups (n=5 each) with end points at 3 and 6 weeks: (1) ischemic control (saline); (2) BDNF (ischemia, 20 μg BDNF); (3) forced arm use (ischemia, saline, and ipsilateral plaster cast …

MaleRestraint PhysicalMotor ActivityLigandsDownregulation and upregulationNeurotrophic factorsForelimbmedicineAnimalsRats WistarReceptorGABA Agonistsalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidStrokePhysical Therapy ModalitiesAdvanced and Specialized NursingBrain-derived neurotrophic factorMuscimolbusiness.industryBrain-Derived Neurotrophic FactorGlutamate receptorBrainCerebral Infarctionmedicine.diseaseRatsUp-RegulationStrokemedicine.anatomical_structureReceptors Glutamatenervous systemAnesthesiaExcitatory postsynaptic potentialAutoradiographyNeurology (clinical)Dizocilpine MaleateIntracranial ThrombosisForelimbCardiology and Cardiovascular MedicinebusinessExcitatory Amino Acid AntagonistsNeuroscienceStroke
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Retrograde neurotrophic signaling in rat retinal ganglion cells is transmitted via the ERK5 but not the ERK1/2 pathway.

2014

Purpose Neurotrophic deprivation is considered an important event in glaucomatous retinal ganglion cell (RGC) death. However, the mitogen-activated protein kinase (MAPK) pathway transmitting axonal neurotrophic signals in RGC has not been identified. We investigated the involvement of ERK5 and ERK1/2 in retrograde axonal neurotrophic signaling in rats. Methods Adult Sprague-Dawley rats were used. Retinal immunostaining for ERK5 and MEK5 was performed. Levels of total and phosphorylated ERK5 and ERK1/2 were analyzed in retinal lysate by quantitative Western blotting. The effects of age, brain-derived neurotrophic factor (BDNF) stimulation at RGC soma (intravitreal injection) or axon ending (…

MaleRetinal Ganglion Cellsmedicine.medical_specialtyAgingSuperior ColliculiMAP Kinase Signaling SystemBlotting WesternRetinal ganglionRetinaRats Sprague-Dawley03 medical and health sciences0302 clinical medicineNeurotrophic factorsInternal medicinemedicineAnimalsAxonPhosphorylationMitogen-Activated Protein Kinase 7030304 developmental biologyBrain-derived neurotrophic factorMitogen-Activated Protein Kinase 10303 health sciencesRetinaMitogen-Activated Protein Kinase 3biologyChemistryBrain-Derived Neurotrophic FactorBrainAnatomyRatsmedicine.anatomical_structureEndocrinologynervous systemRetinal ganglion cellTrk receptorOptic Nerve InjuriesIntravitreal Injectionsbiology.proteinsense organsNeuroglia030217 neurology & neurosurgeryNeurotrophinInvestigative ophthalmologyvisual science
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The interleukin (IL)-31/IL-31R axis contributes to tumor growth in human follicular lymphoma

2014

Interleukin (IL)-31A binds to an heterodimer composed of IL-31 receptor A (IL-31RA) and Oncostatin M Receptor (OSMR). The IL-31/IL-31R complex is involved in the pathogenesis of various skin diseases, including cutaneous T-cell lymphoma. No information is available on the relations between the IL-31/IL-31R complex and B-cell lymphoma. Here we have addressed this issue in follicular lymphoma (FL), a prototypic germinal center(GC)-derived B-cell malignancy. IL-31 enhanced primary FL cell proliferation through IL-31R-driven signal transducer and activator of transcription factor 1/3 (STAT1/3), extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt phosphorylation. In contrast, GC B cells d…

MaleSTAT3 Transcription Factormedicine.medical_specialtyCancer ResearchPrimary Cell CultureFollicular lymphomaBiologyParacrine signallingCytosolCell-Derived MicroparticlesInternal medicinemedicineHumansProtein IsoformsPhosphorylationAutocrine signallingLymphoma FollicularCell ProliferationMitogen-Activated Protein Kinase 1B-LymphocytesMitogen-Activated Protein Kinase 3Gene Expression Regulation LeukemicInterleukinsMicrovesicleMedicine (all)Cell MembraneB-LymphocyteGerminal centerOncostatin M receptorInterleukinProtein IsoformReceptors InterleukinHematologyInterleukinMiddle Agedmedicine.diseaseGerminal CenterMolecular biologyCell-Derived MicroparticleEndocrinologySTAT1 Transcription FactorAnesthesiology and Pain MedicineOncologyFemaleSignal transductionNeoplasm GradingProto-Oncogene Proteins c-aktHumanSignal Transduction
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Cycloastragenol as an Exogenous Enhancer of Chondrogenic Differentiation of Human Adipose-Derived Mesenchymal Stem Cells. A Morphological Study

2020

Stem cell therapy and tissue engineering represent a promising approach for cartilage regeneration. However, they present limits in terms of mechanical properties and premature de-differentiation of engineered cartilage. Cycloastragenol (CAG), a triterpenoid saponin compound and a hydrolysis product of the main ingredient in Astragalus membranaceous, has been explored for cartilage regeneration. The aim of this study was to investigate CAG&rsquo

MaleSettore BIO/17 - IstologiaSapogeninsTime Factorscycloastragenolhuman adipose-derived mesenchymal stem cellsArticleExtracellular matrixchemistry.chemical_compoundTissue engineeringchondrocyte phenotypemedicineHumansCycloastragenolAggrecanscartilage regenerationCell Shapelcsh:QH301-705.5AggrecanCells CulturedGlycoproteinsGlycosaminoglycansCell DeathChemistryCartilageRegeneration (biology)Mesenchymal stem cellCell DifferentiationMesenchymal Stem CellsSOX9 Transcription FactorGeneral MedicineMiddle AgedChondrogenesisCell biologycartilage regeneration; chondrocyte phenotype; cycloastragenol; human adipose-derived mesenchymal stem cells; hypertrophy; tissue engineeringmedicine.anatomical_structurelcsh:Biology (General)tissue engineeringFemaleCollagenhypertrophyChondrogenesiscartilage regeneration; chondrocyte phenotype; cycloastragenol; human adipose-derived mesenchymal stem cells; hypertrophy; tissue engineering; Aggrecans; Cell Death; Cell Differentiation; Cell Shape; Cells Cultured; Chondrogenesis; Collagen; Female; Glycoproteins; Glycosaminoglycans; Humans; Male; Mesenchymal Stem Cells; Middle Aged; SOX9 Transcription Factor; Sapogenins; Time FactorsCells
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