Search results for "blas"

showing 10 items of 2217 documents

DNA replication arrest in response to genotoxic stress provokes early activation of stress-activated protein kinases (SAPK/JNK).

2009

Abstract The impact of DNA damage-induced replication blockage for early activation of stress kinases [stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK)] is largely unknown. Here, we show that induction of dual phosphorylation of SAPK/JNK by the DNA polymerase inhibitor aphidicolin was not ameliorated by additional exposure to ultraviolet (UV) light, indicating that overlapping mechanisms participate in signaling to SAPK/JNK triggered by both agents. UV-induced DNA replication blockage, cyclobutane pyrimidine dimer formation and DNA strand break induction coincided with SAPK/JNK phosphorylation at early (≤ 30 min) but not late (≥ 2 h) time points after exposure. Genotoxin…

AphidicolinDNA ReplicationDNA damageUltraviolet RaysPoly ADP ribose polymeraseCell Linechemistry.chemical_compoundMiceAphidicolinStructural BiologyCricetinaeAnimalsHumansLymphocytesPhosphorylationProtein kinase AMolecular BiologyNucleic Acid Synthesis InhibitorsBRCA2 ProteinMice KnockoutbiologyKinaseCell CycleDNA replicationJNK Mitogen-Activated Protein KinasesFibroblastsMolecular biologyProliferating cell nuclear antigenDNA-Binding ProteinsEnzyme ActivationchemistryPyrimidine Dimersbiology.proteinPhosphorylationApoptosis Regulatory ProteinsDNA DamageJournal of molecular biology
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Neuronal cell cycle: the neuron itself and its circumstances.

2015

Neurons are usually regarded as postmitotic cells that undergo apoptosis in response to cell cycle reactivation. Nevertheless, recent evidence indicates the existence of a defined developmental program that induces DNA replication in specific populations of neurons, which remain in a tetraploid state for the rest of their adult life. Similarly, de novo neuronal tetraploidization has also been described in the adult brain as an early hallmark of neurodegeneration. The aim of this review is to integrate these recent developments in the context of cell cycle regulation and apoptotic cell death in neurons. We conclude that a variety of mechanisms exists in neuronal cells for G1/S and G2/M check…

ApoptosisBrdU 5-bromo-2′-deoxyuridineReviewp75NTR neurotrophin receptor p75Nervous SystemG0 quiescent stateCKI Cdk-inhibitorNeuronsCell DeathNeurodegenerationCell CycleapoptosisNeurodegenerative DiseasesCell cycleCell biologymedicine.anatomical_structureInk inhibitor of kinaseBDNF brain-derived neurotrophic factorp38MAPK p38 mitogen-activated protein kinaseG2 growth phase 2Programmed cell deathS-phasePD Parkinson diseaseRb RetinoblastomaMcm2 minichromosome maintenance 2PCNA proliferating cell nuclear antigenMitosisContext (language use)BiologyCdk cyclin-dependent kinaseCNS central nervous systemS-phase synthesis phase.Cip/Kip cyclin inhibitor protein/kinase inhibitor proteinmedicineAnimalsHumansMolecular BiologyMitosisTetraploidAD Alzheimer diseasecell cycle re-entryDNA replicationCell BiologyNeuronmedicine.diseaseG1 growth phase 1neuronRGCs retinal ganglion cellsCell cycle re-entrytetraploidnervous systemApoptosisNeuronDevelopmental BiologyCell cycle (Georgetown, Tex.)
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Existence and Singularities for the Prandtl Boundary Layer Equations

2000

Prandtl's boundary layer equations, first formulated in 1904, resolve the differences between the viscous and inviscid description of fluid flows. This paper presents a review of mathematical results, both analytic and computational, on the unsteady boundary layer equations. This includes a review of the derivation and basic properties of the equations, singularity formation, well-posedness results, and infinite Reynolds number limits.

Applied MathematicsMathematical analysisPrandtl numberComputational MechanicsReynolds numberBoundary layer thicknessPhysics::Fluid Dynamicssymbols.namesakeBoundary layerInviscid flowBlasius boundary layersymbolsTurbulent Prandtl numberReynolds-averaged Navier–Stokes equationsMathematicsZAMM
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Activation of nitric oxide signaling by the rheumatoid arthritis shared epitope

2006

Objective. Susceptibility to rheumatoid arthritis (RA) is closely associated with HLA–DRB1 alleles encoding a shared epitope (SE) in positions 70–74 of the HLA–DR chain. The mechanistic basis for this association is unknown. Given the proposed pathogenic role of nitric oxide (NO) in RA, this study was undertaken to examine whether the SE can trigger NO signaling events. Methods. The intracellular levels of NO were measured with the fluorescent NO probe 4,5diaminofluorescein diacetate and by the 2,3diaminonaphthalene method. NO synthase activity was determined by measuring the rate of conversion of radioactive arginine to citrulline. Levels of cGMP were measured with a commercial enzyme-link…

ArginineT-LymphocytesMolecular Sequence DataImmunologyCellBiologyNitric OxideEpitopeCell LineNitric oxideArthritis Rheumatoidchemistry.chemical_compoundRheumatologymedicineCitrullineHumansImmunology and AllergyPharmacology (medical)Amino Acid SequenceB cellB-LymphocytesLymphoblastHLA-DR1 AntigenFibroblastsMolecular biologyChromium Radioisotopesmedicine.anatomical_structurechemistryImmunologyEpitopes B-LymphocyteFluoresceinIndicators and ReagentsSignal transductionSignal TransductionArthritis & Rheumatism
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Spontaneous Cardiomyocyte Differentiation From Adipose Tissue Stroma Cells

2004

Cardiomyocyte regeneration is limited in adult life. Thus, the identification of a putative source of cardiomyocyte progenitors is of great interest to provide a usable model in vitro and new perspective in regenerative therapy. As adipose tissues were recently demonstrated to contain pluripotent stem cells, the emergence of cardiomyocyte phenotype from adipose-derived cells was investigated. We demonstrated that rare beating cells with cardiomyocyte features could be identified after culture of adipose stroma cells without addition of 5-azacytidine. The cardiomyocyte phenotype was first identified by morphological observation, confirmed with expression of specific cardiac markers, immunocy…

AtropineMalemedicine.medical_specialtyStromal cellPhysiologyCellular differentiationHeart VentriclesCholinergic AgentsAdipose tissueAdipose tissueCardiomyocytes ; Adipose tissue ; Differentiation ; Stem cells ; Cell therapyStem cellsBiologyCell therapyCell therapyMiceAdrenergic Agents:CIENCIAS MÉDICAS ::Medicina interna [UNESCO]Internal medicinemedicineAnimalsMyocytes CardiacHeart AtriaProgenitor cellInduced pluripotent stem cellCells CulturedUNESCO::CIENCIAS MÉDICAS ::Medicina internaCardiomyocytesRegeneration (biology)Multipotent Stem CellsIsoproterenolCell Differentiation:CIENCIAS MÉDICAS [UNESCO]Myocardial ContractionPropranololCell biologyClone CellsMice Inbred C57BLEndocrinologyPhenotypeAdipose TissueDifferentiationUNESCO::CIENCIAS MÉDICASRNACarbacholStem cellStromal CellsCardiology and Cardiovascular MedicineMyoblasts Cardiac
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Autophagy and apoptosis regolate survival of mesoangioblast stem cells subjected to oxidative stress

2012

Autophagy apoptosis mesoangioblasts oxidative stressSettore BIO/06 - Anatomia Comparata E Citologia
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Características clínicas de los pacientes con LNH del Hospital Arnau de Vilanova de Valencia

2001

Objetivo: Conocer las características clínicas de los pacientes con linfoma no Hodgkin (LNH) en general y por subtipos histológicos atendiendo a la clasificación REAL. Pacientes y métodos: Sobre 210 historias clínicas de pacientes con LNH, se seleccionaron 188 con informe anatomopatológico completo que utilizaban la clasificación REAL o si utilizaban otra clasificación se convirtió a ésta por un experto. Recogiéndose las características clínicas del paciente en el momento del diagnóstico con las que se relacionó. Resultados: Se han encontrado diferencias significativas en la distribución por sexos en los linfomas de células del manto, con predominio de los varones (p= 0,005). Los pacientes …

B Lymphoblastic Lymphomamedicine.medical_specialtybusiness.industryReal classificationLinfoma no HodgkinCaracterísticas clínicasClasificación REALmedicine.diseaseGastroenterologyLymphomaimmune system diseaseshemic and lymphatic diseasesInternal medicineInternal MedicinemedicineStage (cooking)Patient statusbusiness
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1p36 deletion results in a decrease in glycosaminoglycans which is associated with aggressiveness in neuroblastic tumors

2018

Despite our deep understanding of neuroblastic tumors, some patients still suffer treatment failure, so pre-treatment risk stratification still requires improvement and the search for new therapeutic targets must continue. Here we correlated prognostic clinical and biological features of neuroblastic tumors with the density of extracellular matrix glycosaminoglycans (the main components of the extracellular matrix ‘ground substance’), in nearly 400 primary samples. We also studied the relationship between the density of extracellular matrix glycosaminoglycans and the expression of B3GALT6, an enzyme required for their synthesis. We associated a decrease in glycosaminoglycans with neuroblast…

B3GALT6Neuroblastoma1p36 deletionTherapeutic targetHistologia:6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología [CDU]TumorsGlycosaminoglycans
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Bile acid–cysteamine conjugates: Structural properties, gelation, and toxicity evaluation

2011

Abstract Design, synthesis, and characterization of six novel bile acid–cysteamine conjugates together with investigation of their structural studies, gelation properties, and preliminary toxicity evaluation, are reported. Solid state properties of selected compounds were studied by means of X-ray diffraction and 13C CPMAS NMR spectroscopy. N-(2-thioethyl)-3α,7α,12α-trihydroxy-5β-cholan-24-amide was shown to exhibit (pseudo)polymorphism, and a single crystal structure of its non-stoichiometric hydrate is reported herein. Cholyl and dehydrocholyl derivatives bearing three functionalities in their steroidal backbone were shown to undergo self-assembly leading to gelation in certain organic so…

BALB 3T3 CellsMagnetic Resonance Spectroscopymedicine.drug_classCysteamineClinical BiochemistryCholic AcidBiochemistryBile Acids and SaltsInhibitory Concentration 50Micechemistry.chemical_compoundEndocrinologyX-Ray DiffractionmedicineAnimalsOrganic chemistryta116Molecular BiologyPharmacologyBile acidUrsodeoxycholic AcidOrganic ChemistryHydrogen BondingNuclear magnetic resonance spectroscopyFibroblastsAmidesCombinatorial chemistrychemistrySolid-state nuclear magnetic resonancePolymorphism (materials science)SolventsLithocholic AcidCysteamineHydrateSingle crystalDeoxycholic AcidConjugateSteroids
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Translational readthrough of ciliopathy genes BBS2 and ALMS1 restores protein, ciliogenesis and function in patient fibroblasts

2021

Abstract Background Ciliary dysfunction underlies a range of genetic disorders collectively termed ciliopathies, for which there are no treatments available. Bardet-Biedl syndrome (BBS) is characterised by multisystemic involvement, including rod-cone dystrophy and renal abnormalities. Together with Alstrom syndrome (AS), they are known as the ‘obesity ciliopathies’ due to their common phenotype. Nonsense mutations are responsible for approximately 11% and 40% of BBS and AS cases, respectively. Translational readthrough inducing drugs (TRIDs) can restore full-length protein bypassing in-frame premature termination codons, and are a potential therapeutic approach for nonsense-mediated ciliop…

BBS2AdultMaleMedicine (General)AdolescentNonsense mutationAminopyridinesCell Cycle ProteinsCiliopathiesGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundR5-920AtalurenCiliogenesismedicineHumansReceptors SomatostatinBardet-Biedl SyndromeAlstrom SyndromeCells CulturedOxadiazolesbusiness.industryTumor Suppressor ProteinsTranslational readthroughRProteinsGeneral MedicineFibroblastsmedicine.diseaseNonsense suppressionCiliopathiesAtalurenCiliopathyALMS1chemistryCodon NonsenseAmlexanoxCancer researchMedicineBBS2businessAlström syndromeResearch PaperEBioMedicine
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