Search results for "MICE"

showing 10 items of 6027 documents

Loss of rod sensitivity and gene expression changes in the retina of fructose-fed insulin-resistant mice

2012

Purpose: Metabolic syndrome is of major concern in Western countries since it predisposes individuals to the development of diabetes. Insulin resistance is one of the biochemical features of the metabolic syndrome. Fructose feeding has been used to elicit insulin resistance in rodents. Our purpose was to characterize the functional and gene expression changes in the retina after long term feeding mice with a fructose-enriched diet.Methods: Control and ApoB100,LDLR-/- mice, a murine model of aging of the human retina, were fed with a 60%-rich fructose diet for 8 months. Scotopic single flash and Flicker electroretinograms were recorded to monitor the response of the retina to flash stimuli. …

insulin[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologymicelaevulose[ SDV.AEN ] Life Sciences [q-bio]/Food and Nutritionrétinesouris615 nutritional factorseye diseases582 lipidsfructose[SDV.AEN] Life Sciences [q-bio]/Food and Nutrition[SDV.MHEP.OS] Life Sciences [q-bio]/Human health and pathology/Sensory Organs[ SDV.MHEP.OS ] Life Sciences [q-bio]/Human health and pathology/Sensory Organs[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologysense organs[SDV.MHEP.OS]Life Sciences [q-bio]/Human health and pathology/Sensory Organs[SDV.AEN]Life Sciences [q-bio]/Food and Nutritioninsuline[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology532 gene/expressionexpression des gènes
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Golgi Fragmentation in Neurodegenerative Diseases: Is There a Common Cause?

2019

In most mammalian cells, the Golgi complex forms a continuous ribbon. In neurodegenerative diseases, the Golgi ribbon of a specific group of neurons is typically broken into isolated elements, a very early event which happens before clinical and other pathological symptoms become evident. It is not known whether this phenomenon is caused by mechanisms associated with cell death or if, conversely, it triggers apoptosis. When the phenomenon was studied in diseases such as Parkinson’s and Alzheimer’s or amyotrophic lateral sclerosis, it was attributed to a variety of causes, including the presence of cytoplasmatic protein aggregates, malfunctioning of intracellular traffic and/or alterations i…

intracellular transportProgrammed cell deathGolgi ApparatusReviewProtein aggregationBiologyProtein Aggregation Pathologicalsymbols.namesakeMicemedicineAnimalsHumansAmyotrophic lateral sclerosisFragmentation (cell biology)Cytoskeletonlcsh:QH301-705.5NeuronscytoskeletonNeurodegenerative DiseasesGeneral MedicineGolgi apparatusmedicine.diseaseprotein aggregatesGolgi complexlcsh:Biology (General)ApoptosissymbolsNeuroscienceIntracellularCells
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Interpretation of gut microbiota data in the ‘eye of the beholder’: A commentary and re‐evaluation of data from ‘Impacts of radiation exposure on the…

2021

1.Evidence that exposure to environmental pollutants can alter the gut microbiota composition of wildlife includes studies of rodents exposed to radionuclides. 2.Antwis et al. (2021) used amplicon sequencing to characterise the gut microbiota of four species of rodent (Myodes glareolus, Apodemus agrarius, A. flavicollis and A. sylvaticus) inhabiting the Chernobyl Exclusion Zone (CEZ) to examine possible changes in gut bacteria (microbiota) and gut fungi (mycobiota) associated with exposure to radionuclides and whether the sample type (from caecum or faeces) affected the analysis. 3.The conclusions derived from the analyses of gut mycobiota are based on data that represent a mixture of inges…

jyrsijätsuolistomikrobistoTšernobylin ydinonnettomuusAnimals Wilddigestive systemsäteilybiologiaMicemicrobiotaAnimalsradioaktiivinen säteilyluonnonvaraiset eläimetEcology Evolution Behavior and SystematicsMammalsRadioisotopesBacteriaamplicon sequencingArvicolinaedigestive oral and skin physiologyFungiRadiation ExposureGastrointestinal MicrobiomeChernobyl Nuclear Accidentradiation effectsAnimal Science and ZoologyMurinaemycobiotadietMycobiomeJournal of Animal Ecology
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Disturbances in cholesterol, bile acid and glucose metabolism in peroxisomal 3-ketoacylCoA thiolase B deficient mice fed diets containing high or low…

2014

SPE IPM UB; International audience; : The peroxisomal 3-ketoacyl-CoA thiolase B (ThB) catalyzes the thiolytic cleavage of straight chain 3-ketoacyl-CoAs. Up to now, the ability of ThB to interfere with lipid metabolism was studied in mice fed a routinely laboratory chow enriched or not with the synthetic agonist Wy14,643, a pharmacological activator of the nuclear hormone receptor PPARα. The aim of the present study was therefore to determine whether ThB could play a role in obesity and lipid metabolism when mice are chronically fed a synthetic High Fat Diet (HFD) or a Low Fat Diet (LFD) as a control diet. To investigate this possibility, wild-type (WT) mice and mice deficient for Thb (Thb(…

lathosterol.medicine.medical_specialtymedicine.drug_classLathosterolCarbohydrate metabolismBiologyCholesterol 7 alpha-hydroxylaseDiet High-FatBiochemistrylathosterolBile Acids and Saltschemistry.chemical_compoundMiceInternal medicineIntestine Smallmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyInsulin-Like Growth Factor I[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology2. Zero hunger[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismbile acidsBile acidFatty acid metabolismCholesterolCholesterol HDLfood and beveragesLipid metabolismGeneral Medicine[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismAcetyl-CoA C-AcyltransferaseDietary FatsLiver GlycogenEndocrinologyCholesterolGlucosehypoglycemiade novo biosynthesis of cholesterolchemistryGrowth HormoneACOX1lipids (amino acids peptides and proteins)peroxisomal 3-ketoacyl-CoA thiolase B
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Reciprocal influence of B cells and tumor macro and microenvironments in the ApcMin/+ model of colorectal cancer

2017

One of the most fascinating aspects of the immune system is its dynamism, meant as the ability to change and readapt according to the organism needs. Following an insult, we assist to the spontaneous organization of different immune cells which cooperate, locally and at distance, to build up an appropriate response. Throughout tumor progression, adaptations within the systemic tumor environment, or macroenvironment, result in the promotion of tumor growth, tumor invasion and metastasis to distal organs, but also to dramatic changes in the activity and composition of the immune system. In this work, we show the changes of the B-cell arm of the immune system following tumor progression in the…

lcsh:Immunologic diseases. Allergy0301 basic medicineColorectal cancerImmunologySpleenintestinal cancerBiologylcsh:RC254-282Metastasis03 medical and health sciencesImmune systemPeritoneummedicineImmunology and Allergyapcmin/+ miceApcMin/+mice; B lymphocytes; IgA; IL-10; intestinal cancer; Immunology and Allergy; Immunology; OncologyB lymphocyteApcMin/+micelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasePhenotypeInterleukin 10030104 developmental biologymedicine.anatomical_structureOncologyTumor progressionIL-10Immunologyb lymphocyteslcsh:RC581-607IgAOncoImmunology
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Genome-Wide Inhibition of Pro-atherogenic Gene Expression by Multi-STAT Targeting Compounds as a Novel Treatment Strategy of CVDs.

2018

Cardiovascular diseases (CVDs), including atherosclerosis, are globally the leading cause of death. Key factors contributing to onset and progression of atherosclerosis include the pro-inflammatory cytokines Interferon (IFN)a and IFN? and the Pattern Recognition Receptor (PRR) Toll-like receptor 4 (TLR4). Together, they trigger activation of Signal Transducer and Activator of Transcription (STAT)s. Searches for compounds targeting the pTyr-SH2 interaction area of STAT3, yielded many small molecules, including STATTIC and STX-0119. However, many of these inhibitors do not seem STAT3-specific. We hypothesized that multi-STAT-inhibitors that simultaneously block STAT1, STAT2, and STAT3 activit…

lcsh:Immunologic diseases. Allergy0301 basic medicineMaleIn silicoImmunologyGene ExpressionBiologystatIn silico dockingCell LineSmall Molecule Librariessrc Homology Domains03 medical and health sciencesCVDs treatment strategyImmunology and AllergyAnimalsHumansvascular inflammationSTAT1STAT2STAT3Vascular inflammationCells CulturedOriginal ResearchOxadiazolesGene Expression ProfilingSTATPattern recognition receptorin silico dockingFarmaciaAtherosclerosisCyclic S-OxidesMice Inbred C57BLSTAT Transcription Factors030104 developmental biologyCardiovascular DiseasesTLR4biology.proteinSTAT proteinCancer researchQuinolinesmulti-STAT inhibitorsMulti-STAT inhibitorslcsh:RC581-607Genome-Wide Association StudySignal TransductionFrontiers in immunology
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Baseline Gut Microbiota Composition Is Associated With Schistosoma mansoni Infection Burden in Rodent Models

2020

In spite of growing evidence supporting the occurrence of complex interactions between Schistosoma and gut bacteria in mice and humans, no data is yet available on whether worm-mediated changes in microbiota composition are dependent on the baseline gut microbial profile of the vertebrate host. In addition, the impact of such changes on the susceptibility to, and pathophysiology of, schistosomiasis remains largely unexplored. In this study, mice colonized with gut microbial populations from a human donor (HMA mice), as well as microbiota-wild type (WT) animals, were infected with Schistosoma mansoni, and alterations of their gut microbial profiles at 50 days post-infection were compared to …

lcsh:Immunologic diseases. Allergy0301 basic medicineRodentImmunologyAntibodies ProtozoanSchistosomiasisGut floradigestive systemParasite LoadHost-Parasite InteractionsMicrobiologyImmunomodulationFecesMice03 medical and health sciences0302 clinical medicineimmune-modulationhuman-microbiota associated mouse modelsRNA Ribosomal 16Sbiology.animalLactobacillusmedicineAnimalsImmunology and AllergySchistosomaBacteriabiologyFOS: Clinical medicineComputational BiologyBiodiversitySchistosoma mansonidysbiosismedicine.diseasebiology.organism_classificationSchistosomiasis mansoniGastrointestinal MicrobiomeDisease Models Animal030104 developmental biologyhelminth-gut microbiota interactionsSchistosomaMetagenomicsSchistosoma mansonigut microbial diversityProteobacterialcsh:RC581-607Dysbiosis030215 immunology
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A point mutation in the Ncr1 signal peptide impairs the development of innate lymphoid cell subsets.

2018

International audience; NKp46 (CD335) is a surface receptor shared by both human and mouse natural killer (NK) cells and innate lymphoid cells (ILCs) that transduces activating signals necessary to eliminate virus-infected cells and tumors. Here, we describe a spontaneous point mutation of cysteine to arginine (C14R) in the signal peptide of the NKp46 protein in congenic Ly5.1 mice and the newly generated NCR(B6C14R) strain. Ly5.1(C14R) NK cells expressed similar levels of Ncr1 mRNA as C57BL/6, but showed impaired surface NKp46 and reduced ability to control melanoma tumors in vivo. Expression of the mutant NKp46(C14R) in 293T cells showed that NKp46 protein trafficking to the cell surface …

lcsh:Immunologic diseases. Allergy0301 basic medicineSignal peptideintracellular traffickingImmunologyCellCongenicinnate lymphoid cellsBiologymedicine.disease_causelcsh:RC254-28203 medical and health sciences0302 clinical medicinemedicineImmunology and Allergyddc:610congenic miceReceptorOriginal ResearchMutationEndoplasmic reticulumInnate lymphoid cellHEK 293 cellslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensCell biology030104 developmental biologymedicine.anatomical_structureOncologyactivation receptors[SDV.IMM]Life Sciences [q-bio]/Immunologylcsh:RC581-607030215 immunology
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TLR7 controls VSV replication in CD169(+) SCS macrophages and associated viral neuroinvasion

2019

Vesicular stomatitis virus (VSV) is an insect-transmitted rhabdovirus that is neurovirulent in mice. Upon peripheral VSV infection, CD169+ subcapsular sinus (SCS) macrophages capture VSV in the lymph, support viral replication, and prevent CNS neuroinvasion. To date, the precise mechanisms controlling VSV infection in SCS macrophages remain incompletely understood. Here, we show that Toll-like receptor-7 (TLR7), the main sensing receptor for VSV, is central in controlling lymph-borne VSV infection. Following VSV skin infection, TLR7−/− mice display significantly less VSV titers in the draining lymph nodes (dLN) and viral replication is attenuated in SCS macrophages. In contrast to effects o…

lcsh:Immunologic diseases. Allergy0301 basic medicinevirusesImmunologyMedizinDENDRITIC CELLSRIG-IACTIVATION03 medical and health sciences0302 clinical medicinesubcapsular sinus macrophagesSUBCAPSULAR SINUS MACROPHAGESImmunitySIMULIUM-VITTATUM DIPTERAINFECTIONImmunology and Allergyinnate immunityvirus replicationHost factorconditional knock-out miceInnate immune systemScience & TechnologyLYMPH-NODESbiologysubcutaneous infectionPattern recognition receptorpattern recognition receptorsvirus diseasesTLR7VESICULAR STOMATITIS-VIRUSbiology.organism_classificationVirologyddc:Toll-like receptor 7stomatognathic diseases030104 developmental biologyViral replicationVesicular stomatitis virusNEW-JERSEY SEROTYPEINNATE IMMUNITYvesicular stomatitis viruslcsh:RC581-607Viral loadLife Sciences & Biomedicine030215 immunology
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Human γδ T-Cells: From Surface Receptors to the Therapy of High-Risk Leukemias

2018

γδ T lymphocytes are potent effector cells, capable of efficiently killing tumor and leukemia cells. Their activation is mediated by γδ T-cell receptor (TCR) and by activating receptors shared with NK cells (e.g., NKG2D and DNAM-1). γδ T-cell triggering occurs upon interaction with specific ligands, including phosphoantigens (for Vγ9Vδ2 TCR), MICA-B and UL16 binding protein (for NKG2D), and PVR and Nectin-2 (for DNAM-1). They also respond to cytokines undergoing proliferation and release of cytokines/chemokines. Although at the genomic level γδ T-cells have the potential of an extraordinary TCR diversification, in tissues they display a restricted repertoire. Recent studies have identified …

lcsh:Immunologic diseases. Allergy0301 basic medicineαβ T-cellChemokineB-cell depletion; hematopoietic stem cells; HLA-haploidentical transplantation; receptors; αβ T-cell; γδ T-cellsReceptors Antigen T-Cell alpha-betaMini ReviewHLA-haploidentical transplantationImmunologyGenes MHC Class Ichemical and pharmacologic phenomenaMajor histocompatibility complexCD19Mice03 medical and health sciencesγδ T-cellsAntigenReceptorsMHC class ImedicineAnimalsHumansImmunology and AllergyIntraepithelial LymphocytesB-LymphocytesLeukemiaB-cell depletionbiologyT-cell receptorHematopoietic Stem Cell Transplantationmedicine.diseaseNKG2DKiller Cells NaturalLeukemia030104 developmental biologySettore MED/38 - PEDIATRIA GENERALE E SPECIALISTICACytomegalovirus InfectionsImmunologybiology.proteinlcsh:RC581-607Hematopoietic stem cellsFrontiers in Immunology
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