Search results for "MOUSE MODEL"

showing 10 items of 84 documents

Effect of Chemokine Receptors CXCR4 and CCR7 on the Metastatic Behavior of Human Colorectal Cancer

2005

AbstractPurpose: The expression of chemokine receptors CXCR4 and CCR7 has been associated with tumor dissemination and poor prognosis in a limited number of tumor entities. However, no data are currently available on the impact of chemokine receptor expression on disease progression and prognosis in human colorectal cancer.Experimental Design: The expression of CXCR4 and CCR7 was evaluated in 96 patients with histologically confirmed colorectal cancers and in four colorectal cancer cell lines by immunohistochemical staining. Furthermore, cell migration assays were done with SW480, SW620, and LS174T cancer cells to confirm the effect of the CXCR4 ligand stromal cell–derived factor 1α on migr…

MaleReceptors CCR7Receptors CXCR4Cancer ResearchPathologymedicine.medical_specialtyColorectal cancerC-C chemokine receptor type 7Mouse model of colorectal and intestinal cancerMetastasisChemokine receptorCell MovementTumor Cells CulturedHumansMedicineNeoplasm Metastasisbusiness.industryGene Expression ProfilingCancerMiddle AgedPrognosismedicine.diseaseImmunohistochemistryPrimary tumorOncologyLymphatic MetastasisCancer cellDisease ProgressionCancer researchFemaleReceptors ChemokineColorectal NeoplasmsbusinessClinical Cancer Research
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The antidepressant-like effect of tDCS in mice: A behavioral and neurobiological characterization

2017

Abtract Background Transcranial direct current stimulation (tDCS) is a non-invasive method increasingly popular for the treatment of several brain disorders, such as major depression. Despite great enthusiasm and promising results, some studies report discrepant findings and no consensus exists for the clinical use of tDCS. Objective The present study aims to (i) determine the most effective stimulation parameters to optimize antidepressant-like effect of tDCS in the forced-swim test in mice and (ii) identify brain regions recruited by tDCS and possibly involved in its behavioral effect using Fos immunohistochemistry. Results We reported that tDCS induced long-lasting antidepressant-like ef…

MaleStimulation parametersMouse model of depressionmedicine.medical_treatmentBiophysicsPrefrontal CortexAntidepressantStimulationNucleus accumbensTranscranial Direct Current StimulationHippocampuslcsh:RC321-571Mice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCorticosteronemedicineAnimalsPrefrontal cortexlcsh:Neurosciences. Biological psychiatry. NeuropsychiatrySwimmingDepressive Disorder MajorTranscranial direct-current stimulationLong-lasting effectsGeneral NeuroscienceForced-swim test030227 psychiatryMice Inbred C57BLVentral tegmental areamedicine.anatomical_structurechemistryAntidepressantFemaleNeurology (clinical)PsychologyNeuroscience030217 neurology & neurosurgeryBehavioural despair testBrain Stimulation
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Homoarginine Levels are Regulated by L-Arginine: Glycine Amidinotransferase and Affect Stroke Outcome: Results from Human and Murine Studies

2013

Background— Endogenous arginine homologues, including homoarginine, have been identified as novel biomarkers for cardiovascular disease and outcomes. Our studies of human cohorts and a confirmatory murine model associated the arginine homologue homoarginine and its metabolism with stroke pathology and outcome. Methods and Results— Increasing homoarginine levels were independently associated with a reduction in all-cause mortality in patients with ischemic stroke (7.4 years of follow-up; hazard ratio for 1-SD homoarginine, 0.79 [95% confidence interval, 0.64–0.96]; P =0.019; n=389). Homoarginine was also independently associated with the National Institutes of Health Stroke Scale+age score …

Malegenetics [Homoarginine]AmidinotransferasesArginineGenome-wide association studyCohort StudiesMicesingle nucleotide polymorphismMedicinehomoarginineProspective StudiesStrokegenetics [Arginine]CARDIOVASCULAR RISKHazard ratioMOUSE MODELMiddle Ageddiagnosis [Stroke]strokeDEFICIENCYTreatment OutcomeISCHEMIC-STROKEgenetics [Stroke]genetics [Amidinotransferases]genetics [Polymorphism Single Nucleotide]FemaleCardiology and Cardiovascular MedicineAdultmedicine.medical_specialtySingle-nucleotide polymorphismMASS-SPECTROMETRIC DETERMINATIONArginineGUANIDINO COMPOUNDSPhysiology (medical)Internal medicineglycine amidinotransferaseAnimalsHumansCREATINEddc:610Translational research Energy and redox metabolism [ONCOL 3]AgedNITRIC-OXIDEBLOOD-FLOWbusiness.industryVascular diseasemedicine.diseaseHomoarginineCEREBRAL-ARTERY OCCLUSIONL-arginine:glycine amidinotransferaseMice Inbred C57BLDisease Models AnimalEndocrinologyHEK293 CellsGlycinegenome-wide association studiesHuman medicineArginine:glycine amidinotransferasebusinessGenome-Wide Association StudyCirculation
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Impact of Acute and Chronic Amyloid-β Peptide Exposure on Gut Microbial Commensals in the Mouse

2020

Alzheimer’s disease (AD) is the most common form of dementia. Besides its cognitive phenotype, AD leads to crucial changes in gut microbiome composition in model mice and in patients, but the reported data are still highly inconsistent. Therefore, we investigated chronic effects of AD-characteristic neurotoxic amyloid-β (Aβ) peptides as provided by transgenic overexpression (5xFAD mouse model) and acute effects due to oral application of Aβ on gut microbes. Astonishingly, one-time feeding of wild type mice with Aβ42 provoked immediate changes in gut microbiome composition (β diversity) as compared to controls. Such obvious changes were not observed when comparing 5xFAD mice with wild type l…

Microbiology (medical)mouse modelTransgenelcsh:QR1-502microbiomeDiseaseGut floraMicrobiologylcsh:Microbiology03 medical and health sciencesIn vivomedicineMicrobiomeOriginal Research030304 developmental biologyAmyloid-β peptide0303 health sciencesanti-microbialbiology030306 microbiologyWild typebiology.organism_classificationmedicine.disease5xFADPhenotypeImmunologyAlzheimer’s diseaseDysbiosisFrontiers in Microbiology
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Molecular topology as novel strategy for discovery of drugs with aβ lowering and anti-aggregation dual activities for Alzheimer's disease.

2014

Background and Purpose: In this study, we demonstrate the use of Molecular topology (MT) in an Alzheimer's disease (AD) drug discovery program. MT uses and expands upon the principles governing the molecular connectivity theory of numerically characterizing molecular structures, in the present case, active anti-AD drugs/agents, using topological descriptors to build models. Topological characterization has been shown to embody sufficient molecular information to provide strong correlation to therapeutic efficacy. Experimental Approach: We used MT to include multiple bioactive properties that allows for the identification of multifunctional single agent compounds, in this case, the dual func…

Models MolecularDrug Evaluation Preclinicallcsh:MedicineDiseaseProtein aggregationBioinformaticsBiochemistryMechanical Treatment of SpecimensAnimal CellsMolecular Cell BiologyDrug DiscoveryMedicine and Health Scienceslcsh:ScienceTopology (chemistry)NeuronsMultidisciplinaryDrug discoveryMedicine (all)Anti aggregationNeurodegenerative DiseasesAnimal ModelsElectroporationTreatment OutcomeNeurologySpecimen DisruptionDatabases as TopicFemaleMolecular topologyAlzheimer's diseaseCellular TypesResearch ArticleDrug Research and DevelopmentMouse ModelsMice TransgenicComputational biologyBiologyResearch and Analysis MethodsProtein AggregatesModel OrganismsAlzheimer DiseaseMental Health and PsychiatrymedicineAnimalsHumansPharmacologyAmyloid beta-PeptidesBiochemistry Genetics and Molecular Biology (all)lcsh:RBiology and Life SciencesProteinsComputational BiologyCell BiologyDUAL (cognitive architecture)medicine.diseaseDisease Models AnimalAgricultural and Biological Sciences (all)Specimen Preparation and TreatmentFeasibility StudiesDementialcsh:QClinical MedicineProtein MultimerizationPLoS ONE
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Caractérisation des effets ophtalmiques du syndrome de Cohen chez des souris VPS13B-/- et identification des mécanismes moléculaires impliqué dans la…

2020

Cohen Syndrome (CS) is a rare autosomal recessive disease caused by variations in the gene coding for the vacuolar tri-vacuolar protein 13B (VPS13B or COH1). CS patients have common features including typical facial appearance, neutropenia, abnormal trunk fat distribution, microcephaly, myopia and retinal damage. My thesis project aimed to characterize the ophthalmologic phenotype of a mouse model Vps13bEx3/Ex3 to determine the molecular mechanisms involved in the development of CS retinopathy.First, we showed that Vps13bEx3/Ex3 mice develop a cataract between 2 and 3 months. Disorganization of the fibrous cells of the crystalline lens and their differentiation into mesenchymal cells were o…

Mouse ModelModèle Murin[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular Biology[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyCataracteRetinopathyCataractRetinopathie
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Exploratory study on the effects of biodegradable nanoparticles with drugs on malignant B cells and on a human/mouse model of Burkitt lymphoma.

2010

The aim of this study was to determine if Rituximab coated Biodegradable Nanoparticles (BNPs) loaded with Chlorambucil and Hydroxychloroquine could induce apoptosis of B-Chronic Lymphocytic Leukemia (B-CLL), MEC-1 and BJAB cells in vitro and evaluate their toxic and therapeutic effects on a Human/Mouse Model of Burkitt Lymphoma at an exploratory, proof of concept scale. We found that Rituximab-Chlorambucil-Hydroxychloroquine BNPs induce a decrease in cell viability of malignant B cells in a dose-dependent manner. The mediated cytotoxicity resulted from apoptosis, and was confirmed by monitoring the B-CLL cells after Annexin V/propidium iodide staining. Additional data revealed that these BN…

Pathologymedicine.medical_specialtyCell Survivalhuman/mouse model of Burkitt lymphoma.human lymphomamodel SCID mouseAntineoplastic Agentschemistry.chemical_compoundAntibodies Monoclonal Murine-DerivedMicerituximabimmune system diseasesAnnexinhemic and lymphatic diseasesnanoparticles; rituximab; human lymphoma; model SCID mouseTumor Cells CulturedMedicineAnimalsHumansPharmacology (medical)Propidium iodideGeneral Pharmacology Toxicology and PharmaceuticsCytotoxicityB-LymphocytesChlorambucilDose-Response Relationship Drugbusiness.industrymalignant B cellnanoparticleDrug SynergismGeneral MedicineBiodegradable nanoparticles with drugmedicine.diseaseBurkitt LymphomaLymphomaMice Inbred C57BLLeukemiaDisease Models AnimalDrug CombinationschemistryApoptosisMonoclonalCancer researchNanoparticlesChlorambucilbusinessRituximabmedicine.drugHydroxychloroquine
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Hsp60 and Hsp10 as antitumour molecular agents

2007

The molecular chaperones Hsp60 and Hsp10 are, according to recent reports, involved in cancer development and progression. We, for instance, have found that their expression varies with distinctive patterns in different malignancies: they are overexpressed in colorectal, exocervical and prostate carcinogenesis, and colorectal cancer progression, but they are downregulated during bronchial carcinogenesis. There is also evidence showing that Hsp60 and Hsp10 can be used as therapeutic agents, for example in rheumatoid arthritis. In view of these findings we want now to call attention to the potential of Hsp60 and Hsp10 in cancer therapy.

PharmacologyOncologyCancer Researchmedicine.medical_specialtyanimal structuresbusiness.industryColorectal cancermedicine.medical_treatmentfungiCancerImmunotherapyMouse model of colorectal and intestinal cancermedicine.diseasemedicine.disease_causeOncologyRheumatoid arthritisInternal medicineMolecular MedicineMedicineHSP60Cancer developmentbusinessCarcinogenesisCancer Biology & Therapy
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AAV-Mediated Clarin-1 Expression in the Mouse Retina: Implications for USH3A Gene Therapy

2015

Usher syndrome type III (USH3A) is an autosomal recessive disorder caused by mutations in clarin-1 (CLRN1) gene, leading to progressive retinal degeneration and sensorineural deafness. Efforts to develop therapies for preventing photoreceptor cell loss are hampered by the lack of a retinal phenotype in the existing USH3 mouse models and by conflicting reports regarding the endogenous retinal localization of clarin-1, a transmembrane protein of unknown function. In this study, we used an AAV-based approach to express CLRN1 in the mouse retina in order to determine the pattern of its subcellular localization in different cell types. We found that all major classes of retinal cells express AAV…

Photoreceptors0301 basic medicineRetinal degenerationSensory ReceptorsPhysiologyUsher syndromeCell Membraneslcsh:MedicineSocial SciencesNervous SystemPhotoreceptor cellMicechemistry.chemical_compound0302 clinical medicineAnimal CellsMedicine and Health SciencesPsychologylcsh:ScienceNeuronsRegulation of gene expressionGeneticsMultidisciplinaryRetinal DegenerationAnimal ModelsDependovirusCell biologyElectrophysiologymedicine.anatomical_structureSensory PerceptionCellular TypesAnatomyCellular Structures and OrganellesUsher SyndromesResearch ArticleSignal TransductionCell typeImaging TechniquesOcular AnatomyNeurophysiologyOuter plexiform layerMouse ModelsBiologyResearch and Analysis MethodsRetina03 medical and health sciencesModel OrganismsOcular SystemFluorescence ImagingmedicineAnimalsHumansRetinalcsh:RMembrane ProteinsBiology and Life SciencesAfferent NeuronsRetinalGenetic TherapyCell Biologymedicine.diseaseDisease Models Animal030104 developmental biologyGene Expression RegulationchemistrySynapsesEyeslcsh:QHead030217 neurology & neurosurgeryNeurosciencePLOS ONE
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HSP110 promotes colorectal cancer growth through STAT3 activation.

2017

IF 7.932; International audience; Heat shock protein 110 (HSP110) is induced by different stresses and, through its anti-apoptotic and chaperoning properties, helps cells survive these adverse situations. In colon cancers, HSP110 is abnormally abundant. We have recently shown that colorectal cancer patients with microsatellite instability (MSI) had an improved response to chemotherapy because they harbor an HSP110-inactivating mutation (HSP110DE9). In this work, we used patient biopsies, human colorectal cancer cells grown in vitro and in vivo (xenografts), and intestinal crypts to demonstrate that HSP110 is also involved in colon cancer growth. We showed that HSP110 induces colon cancer ce…

STAT3 Transcription Factor0301 basic medicineCancer ResearchColorectal cancerBiopsyMice Nudecolorectal cancer[SDV.CAN]Life Sciences [q-bio]/CancerMouse model of colorectal and intestinal cancerBiologymedicine.disease_causeMolecular oncology[ SDV.CAN ] Life Sciences [q-bio]/CancerSTAT3Mice03 medical and health sciences0302 clinical medicineGrowth factor receptorCell Line TumorGeneticsmedicineAnimalsHumansHSP110 Heat-Shock ProteinsIntestinal MucosaPhosphorylationSTAT3Molecular BiologyCell ProliferationMicrosatellite instabilityCell cyclemedicine.diseaseMolecular biologydigestive system diseases3. Good health030104 developmental biology030220 oncology & carcinogenesisCancer researchbiology.proteinFemaleColorectal NeoplasmsCarcinogenesisNeoplasm TransplantationHSP110Protein Binding
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