Search results for " Disease Models"

showing 10 items of 31 documents

The cholinergic system in Down's syndrome

2006

The cholinergic system is one of the most important modulatory neurotransmitter systems in the brain. Alterations of the transmission communicators are accompanied by reduction of the cortical activity, which is associated with a learning and memory deficit. Down's syndrome is a pathological condition characterized by a high number of abnormalities that involve the brain.The cholinergic system is involved in alterations of the neurological system such as severe learning difficulties.To explain these alterations, important results are obtained from studies about murine trisomy 16 (animal model of Down's syndrome).The results obtained provide useful elements in the improvement of knowledge ab…

030506 rehabilitationDown syndromeCentral nervous systemTrisomyDiseaseSynaptic TransmissionHealth Professions (miscellaneous)Mice03 medical and health sciencesMemorymedicineAnimalsHumansLearningAttentionReceptors Cholinergic0501 psychology and cognitive sciencesDown's syndromePathologicalCerebral CortexHealth PolicyMedicine (all)05 social sciencesCognitive disorderCholinergic systemBrainTrisomy 16medicine.diseaseChromosomes MammalianDevelopmental disorderDisease Models AnimalPsychiatry and Mental healthmedicine.anatomical_structureCholinergic FibersAnimals Attention; physiology Brain; physiopathology Cerebral Cortex; physiopathology Cholinergic Fibers; physiology Chromosomes; Mammalian Disease Models; Animal Down Syndrome; genetics/physiopathology Humans Learning; physiology Memory; physiology Mice Receptors; Cholinergic; physiology Synaptic Transmission; physiology TrisomyIntellectual disabilitieDown Syndrome0305 other medical sciencePsychologyTrisomyNeuroscience050104 developmental & child psychologyJournal of Intellectual Disabilities
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In vivo targeting of human neutralizing antibodies against CD55 and CD59 to lymphoma cells increases the antitumor activity of rituximab.

2007

AbstractAn in vivo model of human CD20+ B-lymphoma was established in severe combined immunodeficiency mice to test the ability of human neutralizing miniantibodies to CD55 and CD59 (MB55 and MB59) to enhance the therapeutic effect of rituximab. The miniantibodies contained single-chain fragment variables and the hinge-CH2-CH3 domains of human IgG1. LCL2 cells were selected for the in vivo study among six B-lymphoma cell lines for their high susceptibility to rituximab-dependent complement-mediated killing enhanced by MB55 and MB59. The cells injected i.p. primarily colonized the liver and spleen, leading to the death of the animals within 30 to 40 days. Thirty percent of mice receiving bio…

Cancer ResearchLymphoma B-Cellmedicine.drug_classmedicine.medical_treatmentAntineoplastic AgentsCD59 AntigensAntigens CD59Mice SCIDPharmacologyMonoclonal antibodyAntigens CD55Antineoplastic AgentAntibodies Monoclonal Murine-DerivedMicerituximabIn vivomedicineAnimalsHumansantibodies against CD55 and CD59CD20Severe combined immunodeficiencyMice Inbred BALB CbiologyCD55 AntigensAnimalAntibody-Dependent Cell CytotoxicityAntibodies MonoclonalImmunotherapyrituximab; antibodies against CD55 and CD59medicine.diseaseDisease Models AnimalOncologyAnimals; Antibodies Monoclonal; Antibodies Monoclonal Murine-Derived; Antibody-Dependent Cell Cytotoxicity; Antigens CD55; Antigens CD59; Antineoplastic Agents; Disease Models Animal; Female; Humans; Lymphoma B-Cell; Mice; Mice Inbred BALB C; Mice SCID; Rituximab; Cancer Research; OncologyMonoclonalImmunologybiology.proteinRituximabFemaleAntibodymedicine.drugHuman
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Spontaneous tumour regression in keratoacanthomas is driven by Wnt/retinoic acid signalling cross-talk

2014

A fundamental goal in cancer biology is to identify the cells and signalling pathways that are keys to induce tumour regression. Here we use a spontaneously self-regressing tumour, cutaneous keratoacanthoma (KAs), to identify physiological mechanisms that drive tumour regression. By using a mouse model system that recapitulates the behaviour of human KAs, we show that self-regressing tumours shift their balance to a differentiation programme during regression. Furthermore, we demonstrate that developmental programs utilized for skin hair follicle regeneration, such as Wnt, are hijacked to sustain tumour growth and that the retinoic acid (RA) signalling pathway promotes tumour regression by …

KeratoacanthomaSkin NeoplasmsRemission SpontaneousRetinoic acidGeneral Physics and AstronomyTretinoinBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health scienceschemistry.chemical_compoundMicePhysics and Astronomy (all)0302 clinical medicineTretinoinStem CellmedicineAnimalsSkin NeoplasmRemission SpontaneouWnt Signaling PathwayAnimals; Carcinoma Squamous Cell; Disease Models Animal; Hair Follicle; Keratoacanthoma; Mice; Remission Spontaneous; Skin Neoplasms; Stem Cells; Tretinoin; Wnt Signaling Pathway; Chemistry (all); Biochemistry Genetics and Molecular Biology (all); Physics and Astronomy (all)030304 developmental biology0303 health sciencesMultidisciplinaryBiochemistry Genetics and Molecular Biology (all)AnimalRegeneration (biology)Stem CellsChemistry (all)Wnt signaling pathwayGeneral Chemistrymedicine.diseaseHair follicleHedgehog signaling pathwayDisease Models AnimalKeratoacanthomamedicine.anatomical_structurechemistry030220 oncology & carcinogenesisImmunologyCancer researchCarcinoma Squamous CellStem cellHair Folliclemedicine.drug
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Hop-derived fraction rich in beta acids and prenylflavonoids regulates the inflammatory response in dendritic cells differently from quercetin: unvei…

2021

Dendritic cells (DCs) represent a heterogeneous family of immune cells that link innate and adaptive immunity and their activation is linked to metabolic changes that are essential to support their activity and function. Hence, targeting the metabolism of DCs represents an opportunity to modify the inflammatory and immune response. Among the natural matrices, Humulus lupulus (Hop) compounds have recently been shown to exhibit immunomodulatory and anti-inflammatory activity. This study aimed to evaluate the ability of specific Hop fractions to modulate DCs metabolism after stimulation with lipopolysaccharide (LPS) by an untargeted metabolomics approach and compare their effect with flavonol …

LipopolysaccharideHop fractions Dendritic cells metabolomics analysis Nrf2/Nqo1 pathwayAnti-Inflammatory AgentsSuccinic AcidInbred C57BLMass SpectrometryProinflammatory cytokineHop (networking)chemistry.chemical_compoundMiceMetabolomicsImmune systemBone MarrowAnimalsMetabolomicsAnimals; Anti-Inflammatory Agents; Bone Marrow; Citrulline; Dendritic Cells; Disease Models Animal; Flavonoids; Humulus; Inflammation; Mass Spectrometry; Metabolomics; Mice; Mice Inbred C57BL; Plant Extracts; Purines; Pyrimidines; Quercetin; Succinic AcidHumulusFlavonoidsInflammationChemistryAnimalPlant ExtractsGeneral MedicineDendritic CellsAcquired immune systemSettore CHIM/08 - Chimica FarmaceuticaCell biologyMice Inbred C57BLDisease Models AnimalPyrimidinesPurinesDisease ModelsCitrullineTumor necrosis factor alphaQuercetinQuercetinFood ScienceFoodfunction
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Immune Cell Toll-like Receptor 4 Mediates the Development of Obesity- and Endotoxemia-Associated Adipose Tissue Fibrosis

2014

International audience; Adipose tissue fibrosis development blocks adipocyte hypertrophy and favors ectopic lipid accumulation. Here, we show that adipose tissue fibrosis is associated with obesity and insulin resistance in humans and mice. Kinetic studies in C3H mice fed a high-fat diet show activation of macrophages and progression of fibrosis along with adipocyte metabolic dysfunction and death. Adipose tissue fibrosis is attenuated by macrophage depletion. Impairment of Toll-like receptor 4 signaling protects mice from obesity-induced fibrosis. The presence of a functional Toll-like receptor 4 on adipose tissue hematopoietic cells is necessary for the initiation of adipose tissue fibros…

LipopolysaccharidesMESH: Signal TransductionMESH: InflammationMESH : Toll-Like Receptor 4Adipose tissueMESH : AdipocytesMESH : LipopolysaccharidesMicechemistry.chemical_compoundFibrosisAdipocyteAdipocytes[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: ObesityMESH: Animalslcsh:QH301-705.5Mice Inbred C3HToll-like receptorMESH : Diet High-FatMESH: Toll-Like Receptor 43. Good healthMESH: Insulin ResistanceAdipose TissueMESH: FibrosisMESH : Fibrosis[SDV.IMM]Life Sciences [q-bio]/ImmunologyMESH : ObesityMESH : Insulin ResistanceMESH: Adipose TissueSignal Transductionmedicine.medical_specialty[SDV.IMM] Life Sciences [q-bio]/ImmunologyAdipose tissue macrophagesBiologyDiet High-FatMESH : Adipose TissueGeneral Biochemistry Genetics and Molecular BiologyImmune systemMESH : Mice Inbred C3HInternal medicineMESH : MicemedicineAnimalsHumansObesityMESH: Mice Inbred C3HMESH: MiceMESH: AdipocytesInflammationMESH : Signal TransductionMESH : InflammationMESH: HumansMESH : EndotoxemiaMESH : Humans3T3-L1medicine.diseaseFibrosisMESH : Disease Models AnimalEndotoxemiaToll-Like Receptor 4Disease Models AnimalMESH: Diet High-FatEndocrinologylcsh:Biology (General)chemistryMESH: EndotoxemiaMESH : AnimalsInsulin ResistanceMESH: Disease Models AnimalMESH: LipopolysaccharidesAdipocyte hypertrophyCell Reports
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Abstract LB-085: A new role for LKB1 to regulate Heat Shock Protein 90 activity

2018

Abstract Approximately 30% of human non-small cell lung cancer (NSCLC) patients harbor a somatic KRAS mutation resulting, in aberrant activation of downstream signaling pathways that control cell proliferation, cell growth, and cell survival. Importantly, alleles of LKB1, a serine/threonine kinase that functions as a tumor suppressor, are somatically inactivated in ~30% of NSCLCs within KRAS-mutant NSCLC. The loss of LKB1 gives rise to aggressive, highly metastatic, and highly drug resistant tumors. We have previously demonstrated that the inactivation of the tumor suppressor lkb1 rendered mutant kras murine NSCLC resistant to targeted agents including BET bromodomain and kinase inhibitors.…

MAPK/ERK pathwaycongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchCell signalingChemistryKinaseCell growthIsogenic human disease modelsOncologyHeat shock proteinCancer researchKinase activityskin and connective tissue diseasesPI3K/AKT/mTOR pathwayCancer Research
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Virulent synergistic effect between Enterococcus faecalis and Escherichia coli assayed by using the Caenorhabditis elegans model.

2008

5 pages; International audience; BACKGROUND: The role of enterococci in the pathogenesis of polymicrobial infections is still debated. The purpose of this study was to evaluate the effect of virulent enterococci in the presence or absence of Escherichia coli strains in the in vivo Caenorhabditis elegans model. PRINCIPAL FINDINGS: This study demonstrated that there was a synergistic effect on virulence when an association of enterococci and E. coli (LT50 = 1.6 days+/-0.1 according to the tested strains and death of nematodes in 4 days+/-0.5) was tested in comparison with enterococci alone (LT50 = 4.6 days+/-0.1 and death in 10.4 days+/-0.6) or E. coli alone (LT50 = 2.1+/-0.9 and deaths 6.6+/…

MESH : Virulence FactorsInfectious Diseases/Gastrointestinal InfectionsMESH : Escherichia colilcsh:MedicineMESH : Genotypemedicine.disease_causeMESH: Regression AnalysisPathogenesisMESH: GenotypeInfectious Diseases/Bacterial InfectionsMESH : Regression AnalysisGenotype[ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/SymbiosisEnterococcus faecalis[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: AnimalsMESH : Anti-Bacterial AgentsMESH : Enterococcus faecalislcsh:ScienceCaenorhabditis elegans0303 health sciencesMultidisciplinarybiologyMESH: Escherichia coliBacterial Infections3. Good healthAnti-Bacterial AgentsMicrobiology/Immunity to InfectionsMESH : Bacterial InfectionsGastroenterology and Hepatology/Gastrointestinal Infections[SDV.IMM]Life Sciences [q-bio]/ImmunologyRegression AnalysisMicrobiology/Cellular Microbiology and PathogenesisResearch ArticleMESH: Enterococcus faecalis[SDV.IMM] Life Sciences [q-bio]/ImmunologyGenotypeMESH: Bacterial InfectionsVirulence FactorsVirulenceEnterococcus faecalisMicrobiologyMESH : Caenorhabditis elegans03 medical and health sciencesIn vivoMESH: Anti-Bacterial AgentsMESH: Caenorhabditis elegansmedicineEscherichia coliAnimalsCaenorhabditis elegansEscherichia coli030304 developmental biologyMESH: Virulence Factors030306 microbiologylcsh:RMicrobiology/Medical Microbiology[SDV.EE.IEO] Life Sciences [q-bio]/Ecology environment/Symbiosisbiology.organism_classificationMESH : Disease Models AnimalDisease Models AnimalEnterococcuslcsh:QMESH : AnimalsMESH: Disease Models Animal[SDV.EE.IEO]Life Sciences [q-bio]/Ecology environment/SymbiosisPloS one
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Toxicity of ligand-dependent Cre recombinases and generation of a conditional Cre deleter mouse allowing mosaic recombination in peripheral tissues.

2007

Ligand-activated Cre recombinases are widely used for studying gene function in vitro and in conditional mouse models. To compare ligand-dependent Cre recombinases, different Cre estrogen receptor fusions were introduced into the ROSA26 locus of embryonic stem (ES) cells and assayed for genotoxicity and recombination efficiency. Of the tested recombinases, the CreERT2 variant showed no toxicity and was highly responsive to ligand induction. To constitutively express CreERT2 in mice and also to clarify whether the CreERT2 system displays background activity, we generated a knock-in mouse line harboring the CreERT2 coding region under the control of the ROSA26 locus. Analysis of this ROSA26-…

MESH: IntegrasesPhysiologyMESH: Mice TransgenicTransgeneMice TransgenicMESH: Flow Cytometry[SDV.CAN]Life Sciences [q-bio]/CancerBiologyLigandsGreen fluorescent proteinMiceMESH: Brain[SDV.CAN] Life Sciences [q-bio]/CancerGenes ReporterGene expressionGeneticsRecombinaseMESH: LigandsAnimalsMESH: AnimalsMESH: Models GeneticGeneMESH: MiceRecombination GeneticIntegrasesModels GeneticMosaicismMESH: GenomicsMESH: Genes ReporterMESH: DNABrainDNAGenomicsFlow CytometryEmbryonic stem cellMolecular biologyPhenotypeDisease Models AnimalMESH: Gene DeletionMESH: Recombination GeneticMESH: MosaicismMESH: Disease Models AnimalFunctional genomicsGene Deletion
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Janus -faced liposomes enhance antimicrobial innate immune response in Mycobacterium tuberculosis infection

2012

We have generated unique asymmetric liposomes with phosphatidylserine (PS) distributed at the outer membrane surface to resemble apoptotic bodies and phosphatidic acid (PA) at the inner layer as a strategy to enhance innate antimycobacterial activity in phagocytes while limiting the inflammatory response. Results show that these apoptotic body-like liposomes carrying PA (ABL/PA) ( i ) are more efficiently internalized by human macrophages than by nonprofessional phagocytes, ( ii ) induce cytosolic Ca 2+ influx, ( iii ) promote Ca 2+ -dependent maturation of phagolysosomes containing Mycobacterium tuberculosis (MTB), ( iv ) induce Ca 2+ -dependent reactive oxygen species (ROS) production, (…

MaleAntitubercular AgentsApoptosisSettore MED/07Mice0302 clinical medicineInnateInbred BALB CMycobacterium tuberculosis liposomes0303 health sciencesMice Inbred BALB CMultidisciplinaryLeukemiaTumorbiologyMacrophages; Leukemia Monocytic Acute; Animals; Apoptosis; Calcium; Humans; Disease Models Animal; Mice; Cell Line Tumor; Immunity Innate; Reactive Oxygen Species; Mice Inbred BALB C; Liposomes; Phosphatidylserines; Tuberculosis Pulmonary; Adult; Bronchoalveolar Lavage Fluid; Middle Aged; Antitubercular Agents; Phagocytosis; Male; Mycobacterium tuberculosis; IsoniazidInterleukinPulmonaryMiddle AgedSettore BIO/193. Good healthPNAS PlusLeukemia Monocytic AcuteTumor necrosis factor alphaBronchoalveolar Lavage FluidIntracellularAdultPhagocytosisPhosphatidylserinesAcutePhagolysosomeSettore MED/07 - MICROBIOLOGIA E MICROBIOLOGIA CLINICAMicrobiologyCell LineMycobacterium tuberculosis03 medical and health sciencesPhagocytosisCell Line TumorIsoniazidTuberculosisAnimalsHumansTuberculosis Pulmonary030304 developmental biologySettore MED/04 - Patologia GeneraletherapyInnate immune systemMonocyticAnimalMacrophagesImmunityMycobacterium tuberculosisbiology.organism_classificationImmunity InnateDisease Models AnimalApoptosisImmunologyDisease ModelsLiposomesCalciumReactive Oxygen Species030215 immunology
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miR-20b and miR-451a Are Involved in Gastric Carcinogenesis through the PI3K/AKT/mTOR Signaling Pathway: Data from Gastric Cancer Patients, Cell Line…

2020

Gastric cancer (GC) is one of the most common and lethal gastrointestinal malignancies worldwide. Many studies have shown that development of GC and other malignancies is mainly driven by alterations of cellular signaling pathways. MicroRNAs (miRNAs) are small noncoding molecules that function as tumor-suppressors or oncogenes, playing an essential role in a variety of fundamental biological processes. In order to understand the functional relevance of miRNA dysregulation, studies analyzing their target genes are of major importance. Here, we chose to analyze two miRNAs, miR-20b and miR-451a, shown to be deregulated in many different malignancies, including GC. Deregulated expression of miR…

MaleCell signalingAntagonists & inhibitorsCaveolin 1ApoptosisCatalysisTuberous Sclerosis Complex 1 ProteinArticleInorganic Chemistrylcsh:ChemistryMicePhosphatidylinositol 3-KinasesStomach NeoplasmsCell Line TumormicroRNAPTENAnimalsHumans616.33-006.6 [udc]Physical and Theoretical ChemistryMolecular BiologyProtein kinase Blcsh:QH301-705.5SpectroscopyPI3K/AKT/mTOR pathwaybiologyTOR Serine-Threonine Kinasesgastric cancerOrganic ChemistryPTEN PhosphohydrolaseAntagomirsGeneral MedicineStomach neoplasms ; genetics ; MicroRNAs ; genetics ; Phosphoinositide-3 Kinase Inhibitors ; Phosphatidylinositol 3-Kinase ; metabolism ; Proto-Oncogene Proteins c-akt ; antagonists&inhibitors ; Proto-Oncogene Proteins c-akt ; metabolism ; TOR Serine-Threonine Kinases ; antagonists&inhibitors ; TOR Serine-Threonine Kinases ; metabolism ; Signal transduction ; drug effects ; Disease models animal ; MicemiR-451aComputer Science ApplicationsmicroRNAsDisease Models Animallcsh:Biology (General)lcsh:QD1-999biology.proteinCancer researchFemalemiR-20bSignal transductionCarrier ProteinsProto-Oncogene Proteins c-aktTXNIPSignal TransductionPI3K/AKT/mTOR signaling pathwayInternational Journal of Molecular Sciences
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