Search results for "Disease Model"

showing 10 items of 1116 documents

Endothelial GLP-1 (Glucagon-Like Peptide 1) Receptor Mediates Cardiovascular Protection by Liraglutide In Mice With Experimental Arterial Hypertension

2019

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0301 basic medicineMalemedicine.medical_specialtyhypertensionBlotting WesternInflammationBlood Pressure030204 cardiovascular system & hematologyangiotensin IImedicine.disease_causeGlucagon-Like Peptide-1 Receptor1005403 medical and health sciencesMice0302 clinical medicine10030Internal medicinemedicineoxidative stressAnimalsHypoglycemic AgentsReceptor10111Cells CulturedMice KnockoutliraglutideLiraglutidebusiness.industryBasic SciencesType 2 Diabetes MellitusEndothelial CellsAtherosclerosisGlucagon-like peptide-1Angiotensin II3. Good healthMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinology10040inflammationComputingMethodologies_DOCUMENTANDTEXTPROCESSINGRNAmedicine.symptomCardiology and Cardiovascular Medicinebusiness10024Oxidative stressmedicine.drug
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Indomethacin counteracts the effects of chronic social defeat stress on emotional but not recognition memory in mice

2017

We have previously observed the impairing effects of chronic social defeat stress (CSDS) on emotional memory in mice. Given the relation between stress and inflammatory processes, we sought to study the effectiveness of the anti-inflammatory indomethacin in reversing the detrimental effects of CSDS on emotional memory in mice. The effects of CSDS and indomethacin on recognition memory were also evaluated. Male CD1 mice were randomly divided into four groups: non-stressed + saline (NS+SAL); non-stressed + indomethacin (NS+IND); stressed + saline (S+SAL); and stressed + indomethacin (S+IND). Stressed animals were exposed to a daily 10 min agonistic confrontation (CSDS) for 20 days. All subjec…

0301 basic medicineMalemedicine.medical_treatmentEmotionsIndomethacinlcsh:MedicineSocial SciencesAnxietySocial defeatMice0302 clinical medicineCognitionLearning and MemoryMedicine and Health SciencesPsychologylcsh:ScienceSalineObject RecognitionMammalsCognitive ImpairmentMultidisciplinaryAnimal BehaviorBehavior AnimalCognitive NeurologyAnti-Inflammatory Agents Non-SteroidalNeurologyAnimal SocialityVertebratesAnxietymedicine.symptomResearch ArticleElevated plus mazemedicine.medical_specialtyCognitive NeurosciencePsychological StressRodents03 medical and health sciencesEmotionalityMemoryInternal medicineMental Health and PsychiatrymedicineAvoidance LearningMemory impairmentAnimalsInterpersonal RelationsRecognition memorySocial stressBehaviorbusiness.industrylcsh:RCognitive PsychologyOrganismsBiology and Life SciencesDisease Models Animal030104 developmental biologyEndocrinologyAmniotesChronic DiseaseCognitive Sciencelcsh:QPerceptionbusinessZoology030217 neurology & neurosurgeryStress PsychologicalNeurosciencePLoS ONE
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EGFL7 enhances surface expression of integrin α5β1 to promote angiogenesis in malignant brain tumors

2018

Abstract Glioblastoma (GBM) is a typically lethal type of brain tumor with a median survival of 15 months postdiagnosis. This negative prognosis prompted the exploration of alternative treatment options. In particular, the reliance of GBM on angiogenesis triggered the development of anti‐VEGF (vascular endothelial growth factor) blocking antibodies such as bevacizumab. Although its application in human GBM only increased progression‐free periods but did not improve overall survival, physicians and researchers still utilize this treatment option due to the lack of adequate alternatives. In an attempt to improve the efficacy of anti‐VEGF treatment, we explored the role of the egfl7 gene in ma…

0301 basic medicineMedicine (General)Vascular Biology & AngiogenesisAngiogenesisEndothelial Growth FactorsQH426-470chemistry.chemical_compoundangiogenesisMice0302 clinical medicineAntineoplastic Agents ImmunologicalResearch ArticlesCancerNeovascularization PathologicBrain NeoplasmsEndothelial stem cellVascular endothelial growth factormedicine.anatomical_structureTreatment Outcome030220 oncology & carcinogenesisendothelial cellMolecular MedicineHeterograftsEGFL7PericyteEGFL7medicine.drugResearch ArticleIntegrin alpha5beta1EGF Family of ProteinsintegrinBrain tumor03 medical and health sciencesR5-920GliomamedicineGeneticsHuman Umbilical Vein Endothelial CellsAnimalsHumansddc:610Cell ProliferationTemozolomidebusiness.industryCalcium-Binding ProteinsglioblastomaEndothelial Cellsmedicine.diseaseSurvival AnalysisDisease Models Animal030104 developmental biologychemistryCancer researchbusinessNeoplasm TransplantationNeuroscienceEMBO Molecular Medicine
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Interleukin 3- receptor targeted exosomes inhibit in vitro and in vivo chronic myelogenous Leukemia cell growth

2017

Despite Imatinib (IM), a selective inhibitor of Bcr-Abl, having led to improved prognosis in Chronic Myeloid Leukemia (CML) patients, acquired resistance and long-term adverse effects is still being encountered. There is, therefore, urgent need to develop alternative strategies to overcome drug resistance. According to the molecules expressed on their surface, exosomes can target specific cells. Exosomes can also be loaded with a variety of molecules, thereby acting as a vehicle for the delivery of therapeutic agents. In this study, we engineered HEK293T cells to express the exosomal protein Lamp2b, fused to a fragment of Interleukin 3 (IL3). The IL3 receptor (IL3-R) is overexpressed in CML…

0301 basic medicineMedicine (miscellaneous)PharmacologyEngineered exosomeExosomesInterleukin 3Antineoplastic AgentMiceHEK293 Cellhemic and lymphatic diseasesDrug CarrierPharmacology Toxicology and Pharmaceutics (miscellaneous)Drug CarriersChronic myeloid leukemiaMyeloid leukemiaChronic myeloid leukemia; Drug delivery; Drug resistance; Engineered exosomes; Interleukin 3; Animals; Antineoplastic Agents; Cell Line Tumor; Cell Proliferation; Disease Models Animal; Drug Carriers; Exosomes; HEK293 Cells; Heterografts; Humans; Imatinib Mesylate; Leukemia Myelogenous Chronic BCR-ABL Positive; Mice; Receptors Interleukin-3; Treatment Outcome3. Good healthTreatment OutcomeImatinib MesylateHeterograftsHeterograftResearch Papermedicine.drugHumanEngineered exosomesAntineoplastic Agents03 medical and health sciencesIn vivoCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineAnimalsHumansneoplasmsInterleukin 3.Interleukin 3Cell Proliferationbusiness.industryAnimalImatinibmedicine.diseaseMicrovesiclesReceptors Interleukin-3ExosomeDisease Models AnimalHEK293 Cells030104 developmental biologyImatinib mesylateDrug resistanceCancer cellDrug deliverybusinessChronic myelogenous leukemia
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Early Cognitive Training Rescues Remote Spatial Memory but Reduces Cognitive Flexibility in Alzheimer’s Disease Mice

2020

Background: Spatial memory dysfunction has been demonstrated in mouse models of Alzheimer’s disease (AD) which is consistent with the clinical finding that the early signature of AD includes difficulties in the formation and/or storage of a memory. A stored memory—a long term memory—can be modulated via process called as memory retrieval that can either lead toward memory reconsolidation or even memory extinction. Objective: We aim to shed light on the fate of the spatial memory during memory reactivation and memory extinction using a water maze task. Methods: In Set-up I, we trained 3-month-old mice (wild-type mice and mice with cerebral β-amyloidosis) and assessed the fate of remote memor…

0301 basic medicineMemory DysfunctionMice TransgenicWater mazecognitive flexibilityExtinction Psychological03 medical and health sciences0302 clinical medicineAlzheimer DiseasemedicineAnimalsmemory retrievalwater mazememory reconsolidationMaze LearningAPP transgeneSpatial MemoryCognitive reserveForgettingOvertrainingbusiness.industryGeneral NeuroscienceCognitive flexibilitymemory extinctionCognitionGeneral Medicinecognitive reservemedicine.diseaseMice Inbred C57BLDisease Models AnimalPsychiatry and Mental healthClinical Psychology030104 developmental biologyMental RecallFemaleMemory consolidationremote memoryGeriatrics and GerontologybusinessAlzheimer’s diseaseNeuroscience030217 neurology & neurosurgeryResearch ArticleJournal of Alzheimer's Disease
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Drosophila melanogaster Models of Metal-Related Human Diseases and Metal Toxicity

2017

Iron, copper and zinc are transition metals essential for life because they are required in a multitude of biological processes. Organisms have evolved to acquire metals from nutrition and to maintain adequate levels of each metal to avoid damaging effects associated with its deficiency, excess or misplacement. Interestingly, the main components of metal homeostatic pathways are conserved, with many orthologues of the human metal-related genes having been identified and characterized in Drosophila melanogaster. Drosophila has gained appreciation as a useful model for studying human diseases, including those caused by mutations in pathways controlling cellular metal homeostasis. Flies have m…

0301 basic medicineMetal toxicityDiseaseComputational biologyReviewCatalysisInorganic Chemistrylcsh:Chemistry03 medical and health sciencesironATP7Metals HeavyMetalloproteinsmedicineAnimalsDrosophila ProteinsToxicologiaPhysical and Theoretical ChemistryMolecular BiologyGeneDrosophilalcsh:QH301-705.5SpectroscopyOrganismMetal Metabolism Inborn ErrorsMetal metabolismfrataxinbiologyEcologyOrganic ChemistryNeurodegenerationzincneurodegenerationGeneral Medicinemedicine.diseasebiology.organism_classificationdZip99CComputer Science ApplicationsDisease Models Animal030104 developmental biologyDrosophila melanogasterlcsh:Biology (General)lcsh:QD1-999coppermetal homeostasisDrosophilaDrosophila melanogasterheavy metal toxicityGenètica
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IL-34–Dependent Intrarenal and Systemic Mechanisms Promote Lupus Nephritis in MRL-Faslpr Mice

2019

Background In people with SLE and in the MRL- Fas lpr lupus mouse model, macrophages and autoantibodies are central to lupus nephritis. IL-34 mediates macrophage survival and proliferation, is expressed by tubular epithelial cells (TECs), and binds to the cFMS receptor on macrophages and to a newly identified second receptor, PTPRZ. Methods To investigate whether IL-34–dependent intrarenal and systemic mechanisms promote lupus nephritis, we compared lupus nephritis and systemic illness in MRL- Fas lpr mice expressing IL-34 and IL-34 knockout (KO) MRL- Fas lpr mice. We also assessed expression of IL-34 and the cFMS and PTPRZ receptors in patients with lupus nephritis. Results Intrarenal IL-3…

0301 basic medicineMice Inbred MRL lprChemokineCell SurvivalLupus nephritisRisk AssessmentMonocytesMice03 medical and health sciences0302 clinical medicineSpecies Specificityimmune system diseasesmedicineAnimalsMacrophageMolecular Targeted Therapyskin and connective tissue diseasesCells CulturedCell ProliferationMice KnockoutSystemic lupus erythematosusCell Deathbiologybusiness.industryInterleukinsMacrophagesGeneral MedicineMonocyte proliferationmedicine.diseaseLupus NephritisMice Inbred C57BLDisease Models AnimalBasic ResearchKidney Tubules030104 developmental biologyGene Expression RegulationNephrology030220 oncology & carcinogenesisImmunologyKnockout mouseDisease Progressionbiology.proteinChemokinesbusinessMacrophage proliferationNephritisJournal of the American Society of Nephrology
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Are moxifloxacin and levofloxacin equally effective to treat XDR tuberculosis?

2017

International audience; Background: Moxifloxacin retains partial activity against some fluoroquinolone-resistant mutants of Mycobacterium tuberculosis. Levofloxacin is presumed to be as active as moxifloxacin against drug-susceptible tuberculosis and to have a better safety profile.Objectives: To compare the in vivo activity of levofloxacin and moxifloxacin against M. tuberculosis strains with various levels of fluoroquinolone resistance.Methods: BALB/c mice were intravenously infected with 106M. tuberculosis H37Rv and three isogenic mutants: GyrA A90V, GyrB E540A and GyrB A543V. Treatment with 50 or 100 mg/kg levofloxacin and 60 or 66 mg/kg moxifloxacin was given orally every 6 h, for 4 we…

0301 basic medicineMicrobiology (medical)Tuberculosis[SDV.SP.MED] Life Sciences [q-bio]/Pharmaceutical sciences/MedicationmiceExtensively Drug-Resistant Tuberculosis030106 microbiologyMicrobial Sensitivity TestsMicrobiologyMycobacterium tuberculosis03 medical and health sciences0302 clinical medicine[SDV.SP.MED]Life Sciences [q-bio]/Pharmaceutical sciences/MedicationLevofloxacinMoxifloxacinIn vivo[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesmedicineAnimalsPharmacology (medical)heterocyclic compounds030212 general & internal medicinePharmacologyMice Inbred BALB ClevofloxacinbiologyChemistry[ SDV.SP.MED ] Life Sciences [q-bio]/Pharmaceutical sciences/MedicationExtensively drug-resistant tuberculosisMycobacterium tuberculosisbiochemical phenomena metabolism and nutritionmedicine.diseasebiology.organism_classificationbacterial infections and mycosesFluoroquinolone resistanceAnti-Bacterial Agents3. Good health[ SDV.MHEP.MI ] Life Sciences [q-bio]/Human health and pathology/Infectious diseasesDisease Models AnimalSafety profileTreatment OutcomeInfectious Diseasestuberculosis[SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseasesbacteriamoxifloxacinFluoroquinolonesmedicine.drug
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Oncogenic Deregulation of EZH2 as an Opportunity for Targeted Therapy in Lung Cancer.

2016

Abstract As a master regulator of chromatin function, the lysine methyltransferase EZH2 orchestrates transcriptional silencing of developmental gene networks. Overexpression of EZH2 is commonly observed in human epithelial cancers, such as non–small cell lung carcinoma (NSCLC), yet definitive demonstration of malignant transformation by deregulated EZH2 remains elusive. Here, we demonstrate the causal role of EZH2 overexpression in NSCLC with new genetically engineered mouse models of lung adenocarcinoma. Deregulated EZH2 silences normal developmental pathways, leading to epigenetic transformation independent of canonical growth factor pathway activation. As such, tumors feature a transcrip…

0301 basic medicineModels MolecularLung Neoplasmsmedicine.medical_treatmentMolecular ConformationGene ExpressionAntineoplastic Agentsmacromolecular substancesBiologymedicine.disease_causeArticleMalignant transformationTargeted therapy03 medical and health sciencesMiceStructure-Activity RelationshipCell Line TumormedicineAnimalsHumansEnhancer of Zeste Homolog 2 ProteinMolecular Targeted TherapyLung cancerPromoter Regions GeneticGene Expression ProfilingEZH2Cancermedicine.diseaseMagnetic Resonance ImagingXenograft Model Antitumor AssaysChromatinrespiratory tract diseasesGene Expression Regulation NeoplasticDisease Models Animal030104 developmental biologyCell Transformation NeoplasticEnhancer Elements GeneticOncologyDrug DesignCancer researchAdenocarcinomaKRASEpigenetic therapyCancer discovery
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rbFOX1/MBNL1 competition for CCUG RNA repeats binding contributes to myotonic dystrophy type 1/type 2 differences

2018

Myotonic dystrophy type 1 and type 2 (DM1, DM2) are caused by expansions of CTG and CCTG repeats, respectively. RNAs containing expanded CUG or CCUG repeats interfere with the metabolism of other RNAs through titration of the Muscleblind-like (MBNL) RNA binding proteins. DM2 follows a more favorable clinical course than DM1, suggesting that specific modifiers may modulate DM severity. Here, we report that the rbFOX1 RNA binding protein binds to expanded CCUG RNA repeats, but not to expanded CUG RNA repeats. Interestingly, rbFOX1 competes with MBNL1 for binding to CCUG expanded repeats and overexpression of rbFOX1 partly releases MBNL1 from sequestration within CCUG RNA foci in DM2 muscle ce…

0301 basic medicineModels MolecularProtein Conformation alpha-Helical[SDV]Life Sciences [q-bio]General Physics and AstronomyGene ExpressionRNA-binding proteinCrystallography X-Raychemistry.chemical_compoundMOLECULAR-BASISGene expressionMBNL1Myotonic DystrophyComputingMilieux_MISCELLANEOUSMultidisciplinaryCHLORIDE CHANNELQRNA-Binding ProteinsRecombinant Proteins3. Good healthCell biologyCONGENITAL HEART-DISEASEDrosophila melanogasterThermodynamicsSKELETAL-MUSCLERNA Splicing FactorsCUG REPEATSProtein BindingRNA Splicing Factorsmusculoskeletal diseasesSTEADY-STATEcongenital hereditary and neonatal diseases and abnormalitiesScienceRBFOX1BiologyMyotonic dystrophyBinding CompetitiveGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesmedicineEscherichia coliAnimalsHumansProtein Interaction Domains and MotifsBinding siteNucleotide MotifsMuscle SkeletalSPLICING REGULATOR RBFOX2MUSCLEBLIND PROTEINSBinding SitesPRE-MESSENGER-RNARNAGeneral Chemistrymedicine.diseaseDisease Models AnimalKinetics030104 developmental biologychemistryTRIPLET REPEATRNAProtein Conformation beta-Strand3111 Biomedicine
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