Search results for "GFA"

showing 10 items of 12 documents

Coexpresión de NG2/GFAP tras la diferenciación en células transfectadas con las mutaciones de GFAP y en células procedentes de gliomas indiferenciados

2020

Resumen: Introducción: La enfermedad de Alexander es una enfermedad rara causada por mutaciones en el gen que codifica la proteína glial ácida fibrilar (GFAP). En un estudio previo hemos observado que la diferenciación de neuroesferas transfectadas con estas mutaciones genera un tipo celular que comparte la expresión de GFAP y NG2. Objetivos: Determinar el efecto de las mutaciones en marcadores moleculares en comparación con células de glioma diferenciados que expresan simultáneamente GFAP y NG2. Métodos: Se utilizaron muestras de glioblastoma humana (GLM) y neuroesferas procedentes de rata transfectadas con mutaciones de GFAP para el análisis de la expresión tras diferenciación de GFAP y N…

0301 basic medicineGFAPmacromolecular substancesGliomalcsh:RC346-42903 medical and health sciences030104 developmental biology0302 clinical medicinenervous systemCaspase-3Alexander diseaseNG2Neurology (clinical)030217 neurology & neurosurgerylcsh:Neurology. Diseases of the nervous systemNeurología
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Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.

2019

Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of…

0301 basic medicineMaleCancer ResearchBiopsyL-amp GB EGFR-low amplified glioblastomamedicine.disease_causewt wildtypeMYBPC3 myosin-binding protein C0302 clinical medicineHIC1 hypermethylated in cancer 1Gene duplicationIn Situ Hybridization FluorescenceIDH2 isocitrate dehydrogenase 2MutationRB-pat RB signaling pathwayEGFRvIII epidermal growth factor receptor variant number IIIPAH phenylalanine hydroxylaseGBM glioblastoma IDH-wildtype (glioblastoma multiforme primary glioblastoma).ANOVA ANalysis Of VArianceN-amp GB EGFR-no amplified glioblastomaMiddle AgedCDKN2A cyclin-dependent kinase inhibitor 2Alcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisPrimary tumorImmunohistochemistryH-amp GB EGFR-high amplified glioblastomaErbB ReceptorsTKR-pat tyrosine-kinase receptors signaling pathway030220 oncology & carcinogenesisDisease ProgressionCDK6 cyclin-dependent kinase 6CDH1 Cadherin 1FemaleCREM cAMP response element modulatorIHC immunohistochemistryAdultOriginal articleDNA Copy Number VariationsCDKN1B cyclin-dependent kinase inhibitor 1BBiologyRARB retinoic acid receptor betaCNS central nervous systemlcsh:RC254-282IDH1 isocitrate dehydrogenase 1BCL2 B-cell cll/ lymphoma 2CNAs copy number algerationsWHO World Health Organization03 medical and health sciencesYoung Adultp53-pat p53 signaling pathwaymedicineBiomarkers TumorTMA tissue microarrayPTENHumansProtein kinase BPI3K/AKT/mTOR pathwaySurvival analysisAgedGenetic heterogeneityGene AmplificationGFAP glial fibrillary acidic proteinMLPA multiplex ligation-dependent probe amplificationmedicine.diseaseFISH fluorescence in situ hibridizationSurvival AnalysisCDKN2B cyclin-dependent kinase inhibitor 2BPTEN phosphatase and tensin homologEGFR epidermal growth factor receptorCNV-load load of copy number variations030104 developmental biologyMutationPARK2 parkinCancer researchbiology.proteinTCGA The Cancer Genome AtlasLARGE1 acetylglucosaminyltransferase-like protein 1GlioblastomaCHD7 Chromodomain Helicase DNA Binding Protein 7DAPI 4′6-diamidino-2-phenylindoleNeoplasia (New York, N.Y.)
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TGF-β Serum Levels in Diabetic Retinopathy Patients and the Role of Anti-VEGF Therapy.

2020

Transforming growth factor &beta

0301 basic medicinePlacental growth factorMaleVascular Endothelial Growth Factor Aserum biomarkersGastroenterologylcsh:ChemistryPathogenesischemistry.chemical_compound0302 clinical medicineTransforming Growth Factor betaMedicineMolecular Targeted Therapylcsh:QH301-705.5SpectroscopyAfliberceptAged 80 and overGeneral MedicineDiabetic retinopathyTGFComputer Science ApplicationsVascular endothelial growth factor ABiomarker (medicine)Intercellular Signaling Peptides and ProteinsFemaleTomography Optical Coherencemedicine.drugmedicine.medical_specialtyanti-VEGFAAnti-VEGFA; Diabetic retinopathy; Serum biomarkers; TGFCatalysisArticleProinflammatory cytokineInorganic Chemistry03 medical and health sciencesTGFβInternal medicineHumansPhysical and Theoretical ChemistryMolecular BiologyAgedDiabetic Retinopathybusiness.industryOrganic Chemistrymedicine.diseaseeye diseases030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistryDiabetes Mellitus Type 2ROC Curve030221 ophthalmology & optometryGlycated hemoglobinbusinessBiomarkersInternational journal of molecular sciences
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Cellular Response to Spinal Cord Injury in Regenerative and Non-Regenerative Stages in Xenopus Laevis

2020

Abstract Background The efficient regenerative abilities at larvae stages followed by a non-regenerative response after metamorphosis in froglets makes Xenopus an ideal model organism to understand the cellular responses leading to spinal cord regeneration. Methods We compared the cellular response to spinal cord injury between the regenerative and non-regenerative stages of Xenopus laevis. For this analysis, we used electron microscopy, immunofluorescence and histological staining of the extracellular matrix. We generated two transgenic lines: i) the reporter line with the zebrafish GFAP regulatory regions driving the expression of EGFP, and ii) a cell specific inducible ablation line with…

0301 basic medicineSpinal Cord RegenerationGfapXenopusNeurogenesislcsh:RC346-429Glial scarGlial scar03 medical and health sciencesXenopus laevis0302 clinical medicineDevelopmental NeuroscienceNeural Stem CellsmedicineAnimalsRegenerationsox2Progenitor cellSpinal cord injuryZebrafishSpinal Cord RegenerationSpinal Cord InjuriesZebrafishlcsh:Neurology. Diseases of the nervous systemSpinal cordbiologyRegeneration (biology)NeurogenesisSpinal cordmedicine.diseasebiology.organism_classificationCell biology030104 developmental biologymedicine.anatomical_structureNSPCsnervous system030217 neurology & neurosurgeryResearch Article
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Susceptibility to Heart Defects in Down Syndrome Is Associated with Single Nucleotide Polymorphisms in HAS 21 Interferon Receptor Cluster and VEGFA G…

2020

Background: Congenital heart defects (CHDs) are present in about 40&ndash

0301 basic medicineVEGFAAdultHeart Defects CongenitalMaleVascular Endothelial Growth Factor ADown syndromelcsh:QH426-470AdolescentChromosomes Human Pair 21Down syndromeSNPSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideArticle03 medical and health sciencesHeart disorder0302 clinical medicineGenotypeGeneticsmedicineHumansGeneGenetics (clinical)IFNRReceptors InterferonGeneticsmedicine.diseasePhenotypeHeart defectlcsh:GeneticsVascular endothelial growth factor A030104 developmental biologySettore MED/03 - Genetica Medica030220 oncology & carcinogenesisMultigene Familyheart defectsFemaleChromosome 21SNPsGenes
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Alexander Disease Mutations Produce Cells with Coexpression of Glial Fibrillary Acidic Protein and NG2 in Neurosphere Cultures and Inhibit Differenti…

2017

Background Alexander disease (AxD) is a rare disease caused by mutations in the gene encoding glial fibrillary acidic protein (GFAP). The disease is characterized by presence of GFAP aggregates in the cytoplasm of astrocytes and loss of myelin. Objectives Determine the effect of AxD-related mutations on adult neurogenesis. Methods We transfected different types of mutant GFAP into neurospheres using the nucleofection technique. Results We find that mutations may cause coexpression of GFAP and NG2 in neurosphere cultures, which would inhibit the differentiation of precursors into oligodendrocytes and thus explain the myelin loss occurring in the disease. Transfection produces cells that diff…

0301 basic medicinecaspase-3Cathepsin Dmacromolecular substancesHSP27lcsh:RC346-429oligodendrocyte precursors03 medical and health sciencesMyelin0302 clinical medicineAlexander diseaseNG2Neurosphereneurospheresmedicinecathepsinlcsh:Neurology. Diseases of the nervous systemOriginal ResearchGlial fibrillary acidic proteinbiologyNeurogenesisNestinGFAP stainmedicine.diseaseMolecular biologyAlexander disease030104 developmental biologymedicine.anatomical_structurenervous systemNeurologyglial fibrillary acidic proteinbiology.proteinNeurology (clinical)030217 neurology & neurosurgeryNeuroscienceFrontiers in Neurology
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Fake Nodes approximation for Magnetic Particle Imaging

2020

Accurately reconstructing functions with discontinuities is the key tool in many bio-imaging applications as, for instance, in Magnetic Particle Imaging (MPI). In this paper, we apply a method for scattered data interpolation, named mapped bases or Fake Nodes approach, which incorporates discontinuities via a suitable mapping function. This technique naturally mitigates the Gibbs phenomenon, as numerical evidence for reconstructing MPI images confirms.

Computer scienceComputingMethodologies_IMAGEPROCESSINGANDCOMPUTERVISIONradial basis functionsFunction (mathematics)Magnetic Particle ImagingClassification of discontinuitieskernelsinterpolationGibbs phenomenonSettore MAT/08 - Analisi Numericasymbols.namesakeMagnetic particle imagingsymbolsKey (cryptography)Radial basis functioninterpolation; kernels; Magnetic Particle Imaging; radial basis functionsGFadial basis functionAlgorithmComputingMethodologies_COMPUTERGRAPHICSInterpolation2020 IEEE 20th Mediterranean Electrotechnical Conference ( MELECON)
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NG2 and GFAP co-expression after differentiation in cells transfected with mutant GFAP and in undifferentiated glioma cells

2020

Introduction: Alexander disease is a rare disorder caused by mutations in the gene coding for glial fibrillary acidic protein (GFAP). In a previous study, differentiation of neurospheres transfected with these mutations resulted in a cell type that expresses both GFAP and NG2. Objective: To determine the effect of molecular marker mutations in comparison to undifferentiated glioma cells simultaneously expressing GFAP and NG2. Methods: We used samples of human glioblastoma (GBM) and rat neurospheres transfected with GFAP mutations to analyse GFAP and NG2 expression after differentiation. We also performed an immunocytochemical analysis of neuronal differentiation for both cell types and dete…

Enfermedad de AlexanderCell typeGlial fibrillary acidic proteinGFAPVimentinGliomamacromolecular substancesTransfectionBiologymedicine.diseaseMolecular biologylcsh:RC346-429Alexander diseaseOLIG203 medical and health sciences0302 clinical medicinenervous systemNG2GliomaNeurospheremedicinebiology.proteinCaspasa 3lcsh:Neurology. Diseases of the nervous system030217 neurology & neurosurgeryNeurología (English Edition)
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Characterization of rodent pineal astrocytes by immunofluorescence microscopy using a monoclonal antibody (J1-31).

1987

In previous studies pineal astrocytes have been characterized immunohistochemically mainly by use of antisera to glial fibrillary acidic protein. Because of the recent demonstration of this protein in non-astrocytic cells the question of its specificity as an astrocytic marker has been raised. A possible alternative tool for characterizing pineal astrocytes is the J1-31 monoclonal antibody, which is directed against a 30 000 dalton astrocytic protein clearly distinguishable from glial fibrillary acidic protein. Immunofluorescence microscopy of this antibody in the pineal gland of rat and guinea-pig revealed a staining pattern similar to that obtained by glial acidic fibrillary protein antis…

Maleendocrine systemHistologymedicine.drug_classGuinea PigsFluorescent Antibody TechniqueMonoclonal antibodyPineal GlandPathology and Forensic MedicinePineal glandmedicineAnimalsHumansAntiserumCerebral CortexGlial fibrillary acidic proteinbiologyAntibodies MonoclonalRats Inbred StrainsCell BiologyGFAP stainMolecular biologyStainingRatsmedicine.anatomical_structurenervous systemAstrocytesbiology.proteinImmunohistochemistryAntibodyGerbillinaeCell and tissue research
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Retention-release equilibrium of aroma compounds in polysaccharide gels: study by quantitative structure-activity/property relationships approach

2010

The nature and amount of constituents in food greatly influence aroma release. Pectins and carrageenans are common used thickeners, but their effect on the release of aroma compounds has been studied more frequently for non- homogeneous products than for thickeners separately. The purpose of this work was to study and compare their respective effects in simple model systems. In this way, the release of 13 aroma compounds was analysed by headspace analysis at equilibrium in pure water, i-carrageenan and pectin gels. To evaluate the influence of the chemical structure of aroma com- pounds on retention/release equilibrium between vapour phase and gels, we used a quantitative structure-activity…

ODORANTQuantitative structure–activity relationshipfood.ingredientPectinChemical structure01 natural scienceschemistry.chemical_compound0404 agricultural biotechnologyfoodQSPRPhase (matter)[SDV.IDA]Life Sciences [q-bio]/Food engineeringOrganic chemistryMoleculeAromabiologyChemistry010401 analytical chemistryfood and beverages04 agricultural and veterinary sciencesGeneral Chemistrybiology.organism_classification040401 food scienceRETENTION-RELEASE0104 chemical sciencesCarrageenanPOLYSACCHARIDE GELSGas chromatographyGFAFood ScienceFlavour and Fragrance Journal
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