Search results for "models"

showing 10 items of 8211 documents

Mesenchymal Transition of High-Grade Breast Carcinomas Depends on Extracellular Matrix Control of Myeloid Suppressor Cell Activity

2016

SummaryThe extracellular matrix (ECM) contributes to the biological and clinical heterogeneity of breast cancer, and different prognostic groups can be identified according to specific ECM signatures. In high-grade, but not low-grade, tumors, an ECM signature characterized by high SPARC expression (ECM3) identifies tumors with increased epithelial-to-mesenchymal transition (EMT), reduced treatment response, and poor prognosis. To better understand how this ECM3 signature is contributing to tumorigenesis, we expressed SPARC in isogenic cell lines and found that SPARC overexpression in tumor cells reduces their growth rate and induces EMT. SPARC expression also results in the formation of a h…

0301 basic medicineMyeloidMDSCGene Expressionmedicine.disease_causeT-Lymphocytes RegulatoryPolyethylene GlycolsExtracellular matrixMiceBreast cancerMyeloid CellsOsteonectinMast Cellslcsh:QH301-705.5Mice KnockoutAntigen PresentationMice Inbred BALB CEMTepithelial to mesenchymal transitionBreast cancer; COX-2; CXCL12; ECM; EMT; G-CSF; GM-CSF; MDSC; SPARC; aminobisphosphonates; cyclooxygenase-2; epithelial to mesenchymal transition; extracellular matrix; granulocyte colony-stimulating factor; granulocyte-macrophage colony-stimulating factor; myeloid-derived suppressor cellsCXCL12Granulocyte macrophage colony-stimulating factormedicine.anatomical_structurecyclooxygenase-2granulocyte-macrophage colony-stimulating factorFemalegranulocyte colony-stimulating factormedicine.drugEpithelial-Mesenchymal Transitionextracellular matrixAntineoplastic AgentsBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaG-CSFGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpithelial–mesenchymal transitionECMMesenchymal stem cellSPARCGM-CSFCOX-2myeloid-derived suppressor cellsXenograft Model Antitumor AssaysIsogenic human disease modelsaminobisphosphonates030104 developmental biologylcsh:Biology (General)CelecoxibDoxorubicinImmunologyCancer researchMyeloid-derived Suppressor CellaminobisphosphonateNeoplasm GradingCarcinogenesisCell Reports
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Sng1 associates with Nce102 to regulate the yeast Pkh–Ypk signalling module in response to sphingolipid status

2016

International audience; All cells are delimited by biological membranes, which are consequently a primary target of stress-induced damage. Cold alters membrane functionality by decreasing lipid fluidity and the activity of membrane proteins. In Saccharomyces cerevisiae, evidence links sphingolipid homeostasis and membrane phospholipid asymmetry to the activity of the Ypk1/2 proteins, the yeast orthologous of the mammalian SGK1-3 kinases. Their regulation is mediated by different protein kinases, including the PDK1 orthologous Pkh1/2p, and requires the function of protein effectors, among them Nce102p, a component of the sphingolipid sensor machinery. Nevertheless, the mechanisms and the act…

0301 basic medicineMyriocinOrm2Saccharomyces-cerevisiaeMembrane propertiesFatty Acids MonounsaturatedGlycogen Synthase Kinase 3Bacteriocins[SDV.IDA]Life Sciences [q-bio]/Food engineeringHomeostasisPhosphorylationMicroscopy ConfocalbiologyEffectorPlasma-membraneActin cytoskeleton[ SDV.IDA ] Life Sciences [q-bio]/Food engineeringPhospholipid translocationTransmembrane proteinCell biologyCold TemperatureBiochemistryP-type atpasesSignal transductionCold stressCell-wall integrityProtein BindingSignal TransductionProteins slm1Saccharomyces cerevisiae ProteinsPhospholipid translocationHigh-pressureSaccharomyces cerevisiaeImmunoblottingFluorescence PolarizationSaccharomyces cerevisiaeSignallingModels Biological3-Phosphoinositide-Dependent Protein Kinases03 medical and health sciencesBudding yeastMolecular BiologySphingolipids030102 biochemistry & molecular biologyTryptophan permeasePhospholipid flippingMembrane ProteinsCell Biologybiology.organism_classificationActin cytoskeletonSphingolipidYeast030104 developmental biologyMembrane proteinMutationPeptidesReactive Oxygen Species
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Approaching Sex Differences in Cardiovascular Non-Coding RNA Research

2020

International audience; Cardiovascular disease (CVD) is the biggest cause of sickness and mortality worldwide in both males and females. Clinical statistics demonstrate clear sex differences in risk, prevalence, mortality rates, and response to treatment for different entities of CVD. The reason for this remains poorly understood. Non-coding RNAs (ncRNAs) are emerging as key mediators and biomarkers of CVD. Similarly, current knowledge on differential regulation, expression, and pathology-associated function of ncRNAs between sexes is minimal. Here, we provide a state-of-the-art overview of what is known on sex differences in ncRNA research in CVD as well as discussing the contributing biol…

0301 basic medicineNcRNAER-BETARNA Untranslatedexperimental modelsreceptorsReviewDisease030204 cardiovascular system & hematologyBioinformaticsCardiovascular Systemlcsh:Chemistry0302 clinical medicineSex hormone-binding globulinlncRNAestrogenMedicinePROMOTER METHYLATIONlcsh:QH301-705.5DNA METHYLATIONSpectroscopyGENE-EXPRESSIONSex CharacteristicsbiologyMortality rateGeneral MedicineMOUSE MODELNon-coding RNA[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system3. Good healthComputer Science ApplicationsHEART-FAILUREESTROGEN-RECEPTOR-ALPHAandrogenvascular cells.vascular cellsCatalysisMICRORNA THERAPEUTICSInorganic Chemistry03 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemmicroRNAAnimalsHumansEpigeneticsPhysical and Theoretical ChemistryX-INACTIVATIONMolecular BiologySocioeconomic statusmiRNAbusiness.industryOrganic ChemistryPOSTMENOPAUSAL HORMONE-THERAPYcardiovascular diseasesSexual dimorphism030104 developmental biologylcsh:Biology (General)lcsh:QD1-999biology.proteinbusinessBiomarkersInternational journal of molecular sciences
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A clustering package for nucleotide sequences using Laplacian Eigenmaps and Gaussian Mixture Model.

2018

International audience; In this article, a new Python package for nucleotide sequences clustering is proposed. This package, freely available on-line, implements a Laplacian eigenmap embedding and a Gaussian Mixture Model for DNA clustering. It takes nucleotide sequences as input, and produces the optimal number of clusters along with a relevant visualization. Despite the fact that we did not optimise the computational speed, our method still performs reasonably well in practice. Our focus was mainly on data analytics and accuracy and as a result, our approach outperforms the state of the art, even in the case of divergent sequences. Furthermore, an a priori knowledge on the number of clust…

0301 basic medicineNematoda01 natural sciencesGaussian Mixture Model[STAT.ML]Statistics [stat]/Machine Learning [stat.ML][MATH.MATH-ST]Mathematics [math]/Statistics [math.ST]ComputingMilieux_MISCELLANEOUScomputer.programming_language[STAT.AP]Statistics [stat]/Applications [stat.AP]Phylogenetic treeDNA ClusteringGenomicsHelminth ProteinsComputer Science Applications[STAT]Statistics [stat]010201 computation theory & mathematics[INFO.INFO-MA]Computer Science [cs]/Multiagent Systems [cs.MA]Data analysisEmbeddingA priori and a posteriori[INFO.INFO-DC]Computer Science [cs]/Distributed Parallel and Cluster Computing [cs.DC]Health Informatics0102 computer and information sciences[INFO.INFO-SE]Computer Science [cs]/Software Engineering [cs.SE]Biology[INFO.INFO-IU]Computer Science [cs]/Ubiquitous Computing03 medical and health sciences[INFO.INFO-CR]Computer Science [cs]/Cryptography and Security [cs.CR]Laplacian EigenmapsAnimalsCluster analysis[SDV.GEN]Life Sciences [q-bio]/GeneticsModels Geneticbusiness.industryPattern recognitionNADH DehydrogenaseSequence Analysis DNAPython (programming language)Mixture model[INFO.INFO-MO]Computer Science [cs]/Modeling and SimulationVisualization030104 developmental biologyComputingMethodologies_PATTERNRECOGNITIONPlatyhelminths[INFO.INFO-ET]Computer Science [cs]/Emerging Technologies [cs.ET]Programming LanguagesArtificial intelligence[INFO.INFO-BI]Computer Science [cs]/Bioinformatics [q-bio.QM]businesscomputerComputers in biology and medicine
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Depleted uranium induces human carcinogenesis involving the immune and chaperoning systems: Realities and working hypotheses

2019

Abstract Cancer is caused by a combination of factors, genetic, epigenetics and environmental. Among the latter, environmental pollutants absorbed by contact, inhalation, or ingestion are major proven or suspected culprits. Depleted uranium (DU) is one of them directly pertinent to the military and civilians working in militarized areas. It is considered a weak carcinogen but its implication in cancer development in exposed individuals is supported by various data. Since not all subjects exposed to DU develop cancer, it is likely that DU-dependent carcinogenesis requires cofactors, such as genetic predisposition and deficiencies of the chaperoning and immune systems. It is of the essence to…

0301 basic medicineNeoplasms Radiation-InducedCarcinogenesisNatural killer cellPreventive measureWorking hypothesisBioinformaticsmedicine.disease_causeRisk AssessmentEpigenesis Genetic03 medical and health sciences0302 clinical medicineImmune systemOccupational ExposureGenetic predispositionmedicineHumansBone marrowDepleted uraniumSkinAir PollutantsChaperoning systemCarcinogenic cofactorbusiness.industryGenetic predispositionMicrobiotaMedicine (all)CancerEnvironmental ExposureGeneral MedicineArmed ConflictsModels Theoreticalmedicine.diseaseEnvironmental pollutantMilitary PersonnelImmune system030104 developmental biologyCarcinogensMolecular chaperoneUraniumEnvironmental PollutantsCancer developmentCarcinogenesisbusiness030217 neurology & neurosurgeryMolecular ChaperonesMedical Hypotheses
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Alterations in reelin and reelin receptors in Down syndrome.

2019

Reelin is an extracellular matrix glycoprotein that modulates synaptic function and plasticity, with a crucial role in neuronal migration. Changes in the expression of this protein have been reported in neurodegenerative diseases, such as Alzheimer's disease (AD). This molecule is produced by Cajal-Retzius neurons during development and by inhibitory neurons in the adult nervous system. Individuals with Down syndrome (DS) present an early development of AD; therefore, we analyzed the alterations in this molecule and its receptors in the murine model for DS Ts65Dn as well as in human with DS. We performed immunofluorescence analysis for reelin and its receptors very-low-density lipoprotein r…

0301 basic medicineNervous systemAdultMaleReceptor expressionCell Adhesion Molecules NeuronalNerve Tissue ProteinsReceptors Cell SurfaceTissue BanksInhibitory postsynaptic potential03 medical and health sciencesMice0302 clinical medicinemedicineAnimalsHumansReelinReceptorLDL-Receptor Related ProteinsAgedTemporal cortexNeuronsExtracellular Matrix ProteinsbiologyCell adhesion moleculeGeneral NeuroscienceSerine EndopeptidasesMiddle AgedTemporal LobeCell biologyDisease Models AnimalReelin Protein030104 developmental biologymedicine.anatomical_structurenervous systemReceptors LDLbiology.proteinDown Syndrome030217 neurology & neurosurgeryLipoproteinNeuroreport
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Two different pathogenic mechanisms, dying-back axonal neuropathy and pancreatic senescence, are present in the YG8R mouse model of Friedreich ataxia

2016

Frataxin (FXN) deficiency causes Friedreich's ataxia (FRDA), a multisystem disorder with neurological and non-neurological symptoms. FRDA pathophysiology combines developmental and degenerative processes of dorsal root ganglia (DRG), sensory nerves, dorsal columns and other central nervous structures. A dying-back mechanism has been proposed to explain the peripheral neuropathy and neuropathology. In addition, affected individuals have non-neuronal symptoms such as diabetes mellitus or glucose intolerance. To go further in the understanding of the pathogenic mechanisms of neuropathy and diabetes associated with the disease, we have investigated the humanized mouse YG8R model of FRDA. By bio…

0301 basic medicineNervous systemAgingPathologylcsh:MedicineMedicine (miscellaneous)Mice0302 clinical medicineImmunology and Microbiology (miscellaneous)Ganglia SpinalInsulin-Secreting CellsInsulin SecretionInsulinMuscle spindleDorsal root gangliaCellular SenescenceDiabetisbiologyMusclesDiabetesAnatomyMitochondria3. Good healthmedicine.anatomical_structureSistema nerviós simpàticDying-back neuropathyPeripheral nervous systemCell senescencemedicine.symptomOxidation-Reductionlcsh:RB1-214Research ArticleSenescencemedicine.medical_specialtyAtaxiaNeuroscience (miscellaneous)Friedreich’s ataxiaNeuropathologyGeneral Biochemistry Genetics and Molecular BiologyPàncreesMalalties del sistema nerviós03 medical and health sciencesPeripheral Nervous Systemlcsh:PathologymedicineAnimalsHumansPancreasIslet of Langerhanslcsh:R302Friedreich's ataxiaNervous system Diseasesmedicine.diseaseAxonsMice Inbred C57BLDisease Models Animal030104 developmental biologyPeripheral neuropathyFriedreich AtaxiaSympathetic nervous systemMutationHumanized mouseFrataxinbiology.proteinEnergy Metabolism030217 neurology & neurosurgeryDisease Models & Mechanisms
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Intrinsic volatility of synaptic connections — a challenge to the synaptic trace theory of memory

2017

According to the synaptic trace theory of memory, activity-induced changes in the pattern of synaptic connections underlie the storage of information for long periods. In this framework, the stability of memory critically depends on the stability of the underlying synaptic connections. Surprisingly however, synaptic connections in the living brain are highly volatile, which poses a fundamental challenge to the synaptic trace theory. Here we review recent experimental evidence that link the initial formation of a memory with changes in the pattern of connectivity, but also evidence that synaptic connections are considerably volatile even in the absence of learning. Then we consider different…

0301 basic medicineNeuronal PlasticityGeneral Neuroscience[SCCO.NEUR]Cognitive science/NeuroscienceModels NeurologicalTheoretical modelsBrain03 medical and health sciences030104 developmental biology0302 clinical medicineAnti-Hebbian learningMemoryNeuroplasticityMetaplasticityNeural PathwaysSynapsesAnimalsHumansLearningPsychologyNeuroscience030217 neurology & neurosurgeryComputingMilieux_MISCELLANEOUSTrace theory
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A stable brain from unstable components: Emerging concepts and implications for neural computation.

2017

Neuroscientists have often described the adult brain in similar terms to an electronic circuit board- dependent on fixed, precise connectivity. However, with the advent of technologies allowing chronic measurements of neural structure and function, the emerging picture is that neural networks undergo significant remodeling over multiple timescales, even in the absence of experimenter-induced learning or sensory perturbation. Here, we attempt to reconcile the parallel observations that critical brain functions are stably maintained, while synapse- and single-cell properties appear to be reformatted regularly throughout adult life. In this review, we discuss experimental evidence at multiple …

0301 basic medicineNeuronsArtificial neural networkGeneral NeuroscienceComputationModels NeurologicalBrainSensory systemSynapse03 medical and health sciences030104 developmental biology0302 clinical medicineModels of neural computationBiological neural networkAnimalsHumansNeural Networks ComputerPsychologyNeuroscience030217 neurology & neurosurgeryDynamic equilibriumElectronic circuitNeuroscience
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Neutrophil extracellular traps impair fungal clearance in a mouse model of invasive pulmonary aspergillosis

2019

Abstract Neutrophil extracellular traps (NETs) are formed by polymorphonuclear neutrophils (PMN) and contribute to the innate host defense by binding and killing bacterial and fungal pathogens. Because NET formation depends on histone hypercitrullination by peptidylarginine deiminase 4 (PAD4), we used PAD4 gene deficient (Pad4-/-) mice in a mouse model of invasive pulmonary aspergillosis (IPA) to address the contribution of NETs to the innate host defense in vivo. After the induction (24 h) of IPA by i.t. infection with Aspergillus fumigatus conidia, Pad4-/- mice revealed lower fungal burden in the lungs, accompanied by less acute lung injury, TNFα and citH3 compared to wildtype controls. T…

0301 basic medicineNeutrophilsImmunologyMedizinApoptosisLung injuryExtracellular TrapsArticleAspergillus fumigatusMicrobiologyMice03 medical and health sciences0302 clinical medicineProtein-Arginine Deiminase Type 4In vivomedicineAnimalsHumansImmunology and Allergyskin and connective tissue diseasesLungInvasive Pulmonary AspergillosisMice KnockoutLungbiologyAspergillus fumigatusWild typeHematologyNeutrophil extracellular trapsbiology.organism_classificationmedicine.diseaseImmunity Innaterespiratory tract diseasesMice Inbred C57BLDisease Models AnimalPneumonia030104 developmental biologymedicine.anatomical_structureCitrullinationTumor necrosis factor alpha030215 immunologyImmunobiology
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