Search results for "57"

showing 10 items of 4186 documents

Reconstruction of Diverse Verrucomicrobial Genomes from Metagenome Datasets of Freshwater Reservoirs

2017

The phylum Verrucomicrobia contains freshwater representatives which remain poorly studied at the genomic, taxonomic, and ecological levels. In this work we present eighteen new reconstructed verrucomicrobial genomes from two freshwater reservoirs located close to each other (Tous and Amadorio, Spain). These metagenomeassembled genomes (MAGs) display a remarkable taxonomic diversity inside the phylum and comprise wide ranges of estimated genome sizes (from 1.8 to 6 Mb). Among all Verrucomicrobia studied we found some of the smallest genomes of the Spartobacteria and Opitutae classes described so far. Some of the Opitutae family MAGs were small, cosmopolitan, with a general heterotrophic met…

0301 basic medicineMicrobiology (medical)Range (biology)030106 microbiologylcsh:QR1-502BiologyMicrobiologyGenomelcsh:Microbiology579 - Microbiología03 medical and health sciencesgenome streamliningCopiotrophfreshwater VerrucomicrobiaCladeGeneOriginal ResearchGeneticsmetagenomicsPhylumVerrucomicrobiabiology.organism_classification030104 developmental biologyrhodopsinMetagenomicsEvolutionary biologynitrogen fixationFrontiers in Microbiology
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Age reduces resistance and tolerance in malaria-infected mice.

2021

7 pages; International audience; Once infected, hosts can rely on two strategies to cope with parasites: fight them (resist the infection) or minimize the damage they induce (tolerate the infection). While there is evidence that aging reduces resistance, how tolerance varies as hosts become old has been barely studied. Here, we used a rodent malaria parasite (Plasmodium yoelii) to investigate whether 2- and 12-month old house mice differ in their capacity to resist and tolerate the infection. We found that 12-month old mice harbored higher parasitemia, showing that age reduces resistance to malaria. Infection-induced deterioration of host health was assessed using red blood cell and body ma…

0301 basic medicineMicrobiology (medical)SenescenceAgingsenescenceRodentAnemia[SDV]Life Sciences [q-bio]030106 microbiologyParasitemiaBiologyParasitemiaMicrobiologyHost-Parasite Interactions03 medical and health sciencesMiceImmunitybiology.animalparasitic diseasesGeneticsmedicineAnimals[SDV.MP.PAR]Life Sciences [q-bio]/Microbiology and Parasitology/ParasitologyMolecular BiologyEcology Evolution Behavior and SystematicsPhysiological PhenomenaDisease ResistanceAge FactorsImmunityPlasmodium yoeliimedicine.diseasebiology.organism_classificationanemia3. Good healthMalaria[SDV] Life Sciences [q-bio]virulenceMice Inbred C57BL030104 developmental biologyInfectious DiseasesImmunology[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleHouse miceDisease SusceptibilityMalariaPlasmodium yoeliiInfection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases
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Enhancement of Antigen Presentation by Deletion of Viral Immune Evasion Genes Prevents Lethal Cytomegalovirus Disease in Minor Histocompatibility Ant…

2020

Hematoablative treatment followed by hematopoietic cell transplantation (HCT) for reconstituting the co-ablated immune system is a therapeutic option to cure aggressive forms of hematopoietic malignancies. In cases of family donors or unrelated donors, immunogenetic mismatches in major histocompatibility complex (MHC) and/or minor histocompatibility (minor-H) loci are unavoidable and bear a risk of graft-vs.-host reaction and disease (GvHR/D). Transient immunodeficiency inherent to the HCT protocol favors a productive reactivation of latent cytomegalovirus (CMV) that can result in multiple-organ CMV disease. In addition, there exists evidence from a mouse model of MHC class-I-mismatched GvH…

0301 basic medicineMicrobiology (medical)nodular inflammatory focus (NIF)murine cytomegalovirusbone marrow transplantation030106 microbiologyImmunologyAntigen presentationlcsh:QR1-502Cytomegaloviruschemical and pharmacologic phenomenaCD8 T cellsBiologyCD8-Positive T-LymphocytesMajor histocompatibility complexMicrobiologylcsh:MicrobiologyMinor Histocompatibility Antigens03 medical and health sciencestransplantation toleranceMiceImmune systemCellular and Infection MicrobiologyAntigenMinor histocompatibility antigenAnimalsgraft-vs.-host disease (GvHD)Immune EvasionAntigen PresentationHematopoietic Stem Cell Transplantationhematopoietic reconstitutionBrief Research ReportHistocompatibilityTransplantationMice Inbred C57BL030104 developmental biologyInfectious DiseasesImmunologyCytomegalovirus Infectionsbiology.proteinCD8Frontiers in Cellular and Infection Microbiology
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The Role of NF-κB Triggered Inflammation in Cerebral Ischemia

2021

Cerebral ischemia is a devastating disease that affects many people worldwide every year. The neurodegenerative damage as a consequence of oxygen and energy deprivation, to date, has no known effective treatment. The ischemic insult is followed by an inflammatory response that involves a complex interaction between inflammatory cells and molecules which play a role in the progression towards cell death. However, there is presently a matter of controversy over whether inflammation could either be involved in brain damage or be a necessary part of brain repair. The inflammatory response is triggered by inflammasomes, key multiprotein complexes that promote secretion of pro-inflammatory cytoki…

0301 basic medicineMini ReviewIschemiaNeurosciences. Biological psychiatry. NeuropsychiatryContext (language use)InflammationBrain damageCervell Ferides i lesionsNeuroprotectionNF-κBcerebral ischemia03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicinemedicinebusiness.industryNeurodegenerationneurodegenerationNF-κBInflammasomemedicine.disease030104 developmental biologychemistryinflammationCellular Neuroscienceneuroprotectionmedicine.symptombusinessOxigen Efectes fisiològicsNeuroscience030217 neurology & neurosurgeryRC321-571medicine.drugFrontiers in Cellular Neuroscience
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Mechanisms of Hierarchical Cortical Maturation

2017

Cortical information processing is structurally and functionally organized into hierarchical pathways, with primary sensory cortical regions providing modality specific information and associative cortical regions playing a more integrative role. Historically, there has been debate as to whether primary cortical regions mature earlier than associative cortical regions, or whether both primary and associative cortical regions mature simultaneously. Identifying whether primary and associative cortical regions mature hierarchically or simultaneously will not only deepen our understanding of the mechanisms that regulate brain maturation, but it will also provide fundamental insight into aspects…

0301 basic medicineMini ReviewSensory systemlcsh:RC321-57103 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinemedicineneocortexpyramidal neurondevelopmentlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryAssociative propertyComputational modelNeocortexmaturationhierarchical maturationBrain maturationInformation processing030104 developmental biologymedicine.anatomical_structureNeural processingCellular modelPsychologyNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Cellular Neuroscience
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Ribosome-Targeting Antibiotics Impair T Cell Effector Function and Ameliorate Autoimmunity by Blocking Mitochondrial Protein Synthesis

2019

Summary While antibiotics are intended to specifically target bacteria, most are known to affect host cell physiology. In addition, some antibiotic classes are reported as immunosuppressive for reasons that remain unclear. Here, we show that Linezolid, a ribosomal-targeting antibiotic (RAbo), effectively blocked the course of a T cell-mediated autoimmune disease. Linezolid and other RAbos were strong inhibitors of T helper-17 cell effector function in vitro, showing that this effect was independent of their antibiotic activity. Perturbing mitochondrial translation in differentiating T cells, either with RAbos or through the inhibition of mitochondrial elongation factor G1 (mEF-G1) progressi…

0301 basic medicineMitochondrial translationmedicine.medical_treatmentT-LymphocytesCellMitochondrionmedicine.disease_causeRibosomemitochondrial translationOxidative PhosphorylationantibioticsAutoimmunityACTIVATIONMice0302 clinical medicineribosome-targetingMedicine and Health SciencesImmunology and AllergyTRANSCRIPTION FACTORMolecular Targeted TherapyMice Knockout0303 health sciencesEffectorExperimental autoimmune encephalomyelitisautoimmunityCell DifferentiationPeptide Elongation Factor GAnti-Bacterial Agents3. Good healthCell biologymitochondriaInfectious DiseasesCytokinemedicine.anatomical_structureRESPIRATION030220 oncology & carcinogenesisEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisT cellImmunologyINHIBITIONT cellsBiologyOXAZOLIDINONEPeptides CyclicArticleMitochondrial Proteins03 medical and health sciencesNAD+medicineAnimalsHumanselongation factor G1030304 developmental biologyAutoimmune diseaseBacteriaLinezolidBiology and Life SciencesPATHWAYSDNANADmedicine.diseaseIn vitroMice Inbred C57BL030104 developmental biologyTh17 CellsArgyrinCHLORAMPHENICOLMEMBRANERibosomesImmunity
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In silico discovery of substituted pyrido[2,3-d]pyrimidines and pentamidine-like compounds with biological activity in myotonic dystrophy models

2016

Myotonic dystrophy type 1 (DM1) is a rare multisystemic disorder associated with an expansion of CUG repeats in mutant DMPK (dystrophia myotonica protein kinase) transcripts; the main effect of these expansions is the induction of pre-mRNA splicing defects by sequestering muscleblind-like family proteins (e.g. MBNL1). Disruption of the CUG repeats and the MBNL1 protein complex has been established as the best therapeutic approach for DM1, hence two main strategies have been proposed: targeted degradation of mutant DMPK transcripts and the development of CUG-binding molecules that prevent MBNL1 sequestration. Herein, suitable CUG-binding small molecules were selected using in silico approach…

0301 basic medicineMolecular biologyPhysiologyMutantMyotonic dystrophyDruggabilitylcsh:Medicine01 natural sciencesBiochemistryPhysical ChemistryMyoblastschemistry.chemical_compoundAnabolic AgentsMedicaments--InteraccióAnimal CellsDrug DiscoveryMedicine and Health SciencesMBNL1Drosophila ProteinsMyotonic Dystrophylcsh:ScienceRNA structureConnective Tissue CellsMultidisciplinaryMolecular StructureOrganic CompoundsStem CellsPhysicsRNA-Binding ProteinsBiological activityPhenotypeClimbingMolecular Docking SimulationNucleic acidsChemistryDrosophila melanogasterBiochemistryGenetic DiseasesConnective TissueRNA splicingPhysical SciencesCellular TypesAnatomyLocomotion57 - BiologiaSignal TransductionResearch ArticleBiotechnologyHydrogen bondingcongenital hereditary and neonatal diseases and abnormalitiesIn silicoPrimary Cell CultureComputational biologyBiology010402 general chemistryMyotonic dystrophyMyotonin-Protein KinaseDrug interactionsSmall Molecule Libraries03 medical and health sciencesStructure-Activity RelationshipmedicineAnimalsHumansRNA MessengerEnllaços d'hidrogenClinical GeneticsChemical PhysicsBiology and life sciencesChemical BondingBiological Locomotionlcsh:ROrganic ChemistryEstructura molecularChemical CompoundsHydrogen BondingCell BiologyFibroblastsmedicine.disease0104 chemical sciencesBenzamidinesAlternative SplicingDisease Models AnimalMacromolecular structure analysis030104 developmental biologyPyrimidinesBiological TissuechemistrySmall MoleculesRNAlcsh:QTrinucleotide Repeat ExpansionMolecular structure
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Myeloid cell populations and fibrogenic parameters in bleomycin- and HOCl-induced fibrosis

2016

Mouse models resembling systemic sclerosis can be chemically induced by application of bleomycin or hypochloric acid (HOCl). To date, little is known about inflammatory cells and their potential role in scleroderma (Scl)-related fibrosis. Therefore, we compared both Scl models to define the early immune cell subsets in relation to fibrosis-related parameters. Both agents induced a significant increase in dermal thickness and collagen deposition after 4 weeks, as hallmarks of Scl. However, clinical skin thickness, densely packed, sirius red-stained collagen bundles and collagen cross-links were more pronounced in HOCl-induced Scl. In parallel, there was a significant upregulation of procolla…

0301 basic medicineMyeloidCD11cDermatologyBleomycinBiochemistryCD19Bleomycin03 medical and health scienceschemistry.chemical_compoundImmune systemFibrosishemic and lymphatic diseasesmedicineAnimalsMyeloid CellsMolecular BiologySkinScleroderma Systemicbiologymedicine.diseaseFibrosisMolecular biologyHypochlorous AcidMice Inbred C57BLDisease Models AnimalProcollagen peptidase030104 developmental biologymedicine.anatomical_structurechemistryIntegrin alpha Mbiology.proteinFemaleExperimental Dermatology
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Myeloid cell-synthesized coagulation Factor X dampens anti-tumor immunity

2019

Immune evasion in the tumor microenvironment (TME) is a crucial barrier for effective cancer therapy, and plasticity of innate immune cells may contribute to failures of targeted immunotherapies. Here, we show that rivaroxaban, a direct inhibitor of activated coagulation factor X (FX), promotes antitumor immunity by enhancing infiltration of dendritic cells and cytotoxic T cells at the tumor site. Profiling FX expression in the TME identifies monocytes and macrophages as crucial sources of extravascular FX. By generating mice with immune cells lacking the ability to produce FX, we show that myeloid cell-derived FX plays a pivotal role in promoting tumor immune evasion. In mouse models of ca…

0301 basic medicineMyeloidmedicine.medical_treatmentImmunologyCellMammary Neoplasms AnimalArticle03 medical and health sciencesMice0302 clinical medicineImmune systemmedicineCytotoxic T cellAnimalsHumansMyeloid CellsTumor microenvironmentInnate immune systembusiness.industryGeneral MedicineImmunotherapyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisFactor XCancer researchFemaleImmunotherapySignal transductionbusiness
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Nrf2 expression driven by Foxp3 specific deletion of Keap1 results in loss of immune tolerance in mice

2020

European journal of immunology 50(4), 515-524 (2020). doi:10.1002/eji.201948285

0301 basic medicineNF-E2-Related Factor 2T cellImmunologyAutoimmunitychemical and pharmacologic phenomenaBiologyLymphocyte ActivationT-Lymphocytes Regulatorydigestive systemenvironment and public healthImmune toleranceImmunomodulationMice03 medical and health sciences0302 clinical medicineImmune systemImmune TolerancemedicineAnimalsHomeostasisImmunology and AllergyTranscription factorPI3K/AKT/mTOR pathwayInflammationMice KnockoutKelch-Like ECH-Associated Protein 1ChimeraEffectorTOR Serine-Threonine KinasesPeripheral toleranceFOXP3Forkhead Transcription Factorshemic and immune systemsrespiratory systemCell biologyMice Inbred C57BLOxidative Stress030104 developmental biologymedicine.anatomical_structure030215 immunology
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