Search results for "ddc:616.07"

showing 10 items of 22 documents

Global prevalence, treatment, and prevention of hepatitis B virus infection in 2016: a modelling study

2018

PubMed: 29599078

0301 basic medicineBIOMEDICINE AND HEALTHCARE. Clinical Medical Sciences.HBsAgPediatricsDelphi TechniqueInfectious Disease TransmissionCHRONIC HBV INFECTION ; NATURAL-HISTORY ; FOLLOW-UP ; HBSAG ; CARRIERS ; AGE ; COUNTRIES ; DISEASE ; ANTIGEN ; COHORTddc:616.07Global Healthmedicine.disease_causeDISEASE0302 clinical medicinePrevalenceHBVChildddc:616Antiviral Agents/therapeutic useeducation.field_of_studyBIOMEDICINA I ZDRAVSTVO. Kliničke medicinske znanosti.Chronic/drug therapy/epidemiology/prevention & control/transmissionGastroenterologyHepatitis B Surface Antigens/bloodHepatitis BCARRIERSHepatitis B10219 Clinic for Gastroenterology and HepatologyChild Preschool030211 gastroenterology & hepatologyViral hepatitisViral loadCOUNTRIESAdultmedicine.medical_specialtyHepatitis B vaccineANTIGENPopulation610 Medicine & healthAntiviral AgentsMass VaccinationHepatology; Gastroenterology03 medical and health sciencesHepatitis B ChronicHBSAGAGESDG 3 - Good Health and Well-beingmedicineHumansCOHORT2715 GastroenterologyPreschooleducationDisease burdenHepatitis B virusHepatitis B Surface AntigensHepatologybusiness.industryViral VaccinesNATURAL-HISTORYmedicine.diseaseInfectious Disease Transmission VerticalCHRONIC HBV INFECTIONVertical/prevention & control030104 developmental biology2721 HepatologyHuman medicineFOLLOW-UPbusiness
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Interferon-γ-Driven iNOS: A Molecular Pathway to Terminal Shock in Arenavirus Hemorrhagic Fever

2017

Arenaviruses such as Lassa virus (LASV) cause hemorrhagic fever. Terminal shock is associated with a systemic cytokine storm, but the mechanisms are ill defined. Here we used HLA-A2-expressing mice infected with a monkey-pathogenic strain of lymphocytic choriomeningitis virus (LCMV-WE), a close relative of LASV, to investigate the pathophysiology of arenavirus hemorrhagic fever (AHF). AHF manifested as pleural effusions, edematous skin swelling, and serum albumin loss, culminating in hypovolemic shock. A characteristic cytokine storm included numerous pro-inflammatory cytokines and nitric oxide (NO) metabolites. Edema formation and terminal shock were abrogated in mice lacking inducible nit…

0301 basic medicineMaleHemorrhagic Fevers ViralNitric Oxide Synthase Type IIBiologyLymphocytic Choriomeningitisddc:616.07Lymphocytic choriomeningitismedicine.disease_causeNitric OxideMicrobiologyViral hemorrhagic fever03 medical and health sciencesInterferon-gammaMice0302 clinical medicineVirologymedicineAnimalsHumansLymphocytic choriomeningitis virusLassa feverArenavirusddc:617medicine.diseasebiology.organism_classification3. Good healthNitric oxide synthaseMice Inbred C57BLDisease Models Animal030104 developmental biologyLassa virus030220 oncology & carcinogenesisShock (circulatory)Immunologybiology.proteinParasitologyFemalemedicine.symptomCytokine storm
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Eomes broadens the scope of CD8 T-cell memory by inhibiting apoptosis in cells of low affinity.

2020

The memory CD8 T-cell pool must select for clones that bind immunodominant epitopes with high affinity to efficiently counter reinfection. At the same time, it must retain a level of clonal diversity to allow recognition of pathogens with mutated epitopes. How the level of diversity within the memory pool is controlled is unclear, especially in the context of a selective drive for antigen affinity. We find that preservation of clones that bind the activating antigen with low affinity depends on expression of the transcription factor Eomes in the first days after antigen encounter. Eomes is induced at low activating signal strength and directly drives transcription of the prosurvival protein…

0301 basic medicinePhysiologyAntigenic Variation/immunologyApoptosisCD8 memory viral infection Eomesddc:616.07CD8-Positive T-LymphocytesLymphocyte ActivationEpitopeMemory T cellsMice0302 clinical medicineSpectrum Analysis TechniquesCognitionLearning and MemoryTranscription (biology)Immune PhysiologyReceptorsCellular typesCytotoxic T cellBiology (General)ReceptorClonal Selection Antigen-MediatedCell Survival/immunologyT-Cell/genetics/immunologyT-Lymphoid/immunologyCells CulturedFluorescence-Activated Cell SortingCulturedGeneral NeuroscienceImmune cellsFlow CytometryAntigenic VariationCell biologyProto-Oncogene Proteins c-bcl-2SpectrophotometryAntigenWhite blood cellsT-Box Domain Proteins/genetics/immunologyCytophotometrySignal transductionBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.General Agricultural and Biological SciencesApoptosis/immunologySignal TransductionResearch ArticleCell biologyBlood cellsQH301-705.5Precursor CellsCell SurvivalCellsImmunologyClonal SelectionReceptors Antigen T-CellT cellsCytotoxic T cellsBiologyCD8-Positive T-Lymphocytes/immunologyResearch and Analysis MethodsGeneral Biochemistry Genetics and Molecular BiologyAntigen-Mediated/genetics/immunology03 medical and health sciencesAntigenMemoryAnimalsMolecular Biology TechniquesTranscription factorMolecular BiologyMedicine and health sciencesPrecursor Cells T-LymphoidGene Expression Regulation/immunologyGeneral Immunology and MicrobiologyBiology and life sciencesBIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.T-cell receptorProto-Oncogene Proteins c-bcl-2/genetics/immunology030104 developmental biologyGene Expression RegulationAnimal cellsCognitive ScienceT-Box Domain ProteinsImmunologic Memory030217 neurology & neurosurgerySpleenCloningNeurosciencePLoS biology
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European contribution to the study of ROS : A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

2017

WOS: 000410470000009

0301 basic medicinereactive oxygen species ; reactive nitrogen species ; redox signaling ; oxidative stress ; antioxidants ; redox therapeuticsRedox signalingInternational CooperationSMOOTH-MUSCLE-CELLS[SDV]Life Sciences [q-bio]Clinical BiochemistryISCHEMIA-REPERFUSION INJURYReviewddc:616.07Bioinformaticsmedicine.disease_causeBiochemistryAntioxidants0302 clinical medicineENDOPLASMIC-RETICULUM STRESSCost actionlcsh:QH301-705.5ComputingMilieux_MISCELLANEOUSmedia_commonlcsh:R5-920Redox therapeuticsReactive nitrogen species3. Good healthVariety (cybernetics)MANGANESE SUPEROXIDE-DISMUTASECHRONIC GRANULOMATOUS-DISEASERisk analysis (engineering)ddc:540lcsh:Medicine (General)Oxidation-ReductionSignal TransductionSocieties ScientificPULMONARY ARTERIAL-HYPERTENSIONMedicinaEstrès oxidatiuBiology03 medical and health sciencesAntioxidants ; Oxidative Stress ; Reactive Nitrogen Species ; Reactive Oxygen Species ; Redox Signaling ; Redox TherapeuticsJournal Articlemedicinemedia_common.cataloged_instanceAnimalsHumans[CHIM]Chemical SciencesEuropean UnionEuropean unionNITRIC-OXIDE SYNTHASETANDEM MASS-SPECTROMETRYMolecular BiologyMITOCHONDRIAL OXIDATIVE STRESSGROWTH-FACTOR-BETAOrganic ChemistryDisease progressionBiology and Life SciencesOxidation reductionManganese Superoxide Dismutase030104 developmental biologylcsh:Biology (General)Oxidative stressReactive oxygen species030217 neurology & neurosurgeryOxidative stressRedox biology
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Meta-analysis of real-time fMRI neurofeedback studies using individual participant data: How is brain regulation mediated?

2015

An increasing number of studies using real-time fMRI neurofeedback have demonstrated that successful regulation of neural activity is possible in various brain regions. Since these studies focused on the regulated region(s), little is known about the target-independent mechanisms associated with neurofeedback-guided control of brain activation, i.e. the regulating network. While the specificity of the activation during self-regulation is an important factor, no study has effectively determined the network involved in self-regulation in general. In an effort to detect regions that are responsible for the act of brain regulation, we performed a post-hoc analysis of data involving different ta…

2805 Cognitive NeuroscienceVentrolateral prefrontal cortexBrain regulationCognitive NeuroscienceStress-related disorders Donders Center for Medical Neuroscience [Radboudumc 13]610 Medicine & healthCIBM-SPCddc:616.0757Brain mapping050105 experimental psychologyProcedural memory03 medical and health sciences0302 clinical medicineBasal gangliamedicineHumans0501 psychology and cognitive sciencesAnterior cingulate cortexBrain Mapping05 social sciencesBrainCognitionNeurofeedbackMagnetic Resonance Imagingmedicine.anatomical_structureNeurofeedback Real-time fMRI Brain regulationNeurology10054 Clinic for Psychiatry Psychotherapy and Psychosomatics2808 NeurologyMeta-analysisReal-time fMRINeurofeedbackPsychologyNeuroscience030217 neurology & neurosurgeryBrain Regulation ; Neurofeedback ; Real-time FmriNeuroImage
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SOCS3 transactivation by PPARγ prevents IL-17-driven cancer growth.

2013

Abstract Activation of the transcription factor PPARγ by the n-3 fatty acid docosahexaenoic acid (DHA) is implicated in controlling proinflammatory cytokine secretion, but the intracellular signaling pathways engaged by PPARγ are incompletely characterized. Here, we identify the adapter-encoding gene SOCS3 as a critical transcriptional target of PPARγ. SOCS3 promoter binding and gene transactivation by PPARγ was associated with a repression in differentiation of proinflammatory T-helper (TH)17 cells. Accordingly, TH17 cells induced in vitro displayed increased SOCS3 expression and diminished capacity to produce interleukin (IL)-17 following activation of PPARγ by DHA. Furthermore, naïve CD4…

CD4-Positive T-LymphocytesCancer ResearchAngiogenesisMammary Neoplasms Experimental/genetics/pathology/prevention & controlSuppressor of Cytokine Signaling Proteinsddc:616.07BioinformaticsTransactivationMice0302 clinical medicineTumor Burden/drug effects/geneticsSOCS3Docosahexaenoic Acids/administration & dosage/pharmacologyPromoter Regions GeneticMice Knockout0303 health sciencesMice Inbred BALB CChemistryReverse Transcriptase Polymerase Chain ReactionInterleukin-17InterleukinCell DifferentiationCell biologyTumor BurdenOncology030220 oncology & carcinogenesisFemaleRNA InterferenceInterleukin 17Th17 Cells/drug effects/metabolismTranscriptional ActivationDocosahexaenoic AcidsBlotting WesternMice NudeCD4-Positive T-Lymphocytes/drug effects/metabolismProinflammatory cytokine03 medical and health sciencesSuppressor of Cytokine Signaling Proteins/genetics/metabolismCell Line TumorAnimalsTranscription factor030304 developmental biologyMammary Neoplasms ExperimentalPromoter Regions Genetic/geneticsDietMice Inbred C57BLPPAR gammaInterleukin-17/metabolismCell cultureSuppressor of Cytokine Signaling 3 ProteinCell Differentiation/drug effectsPPAR gamma/agonists/genetics/metabolismTh17 CellsCancer research
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IkappaB kinase 2 determines oligodendrocyte loss by non-cell-autonomous activation of NF-kappaB in the central nervous system

2011

The IκB kinase complex induces nuclear factor kappa B activation and has recently been recognized as a key player of autoimmunity in the central nervous system. Notably, IκB kinase/nuclear factor kappa B signalling regulates peripheral myelin formation by Schwann cells, however, its role in myelin formation in the central nervous system during health and disease is largely unknown. Surprisingly, we found that brain-specific IκB kinase 2 expression is dispensable for proper myelin assembly and repair in the central nervous system, but instead plays a fundamental role for the loss of myelin in the cuprizone model. During toxic demyelination, inhibition of nuclear factor kappa B activation by …

Central Nervous SystemBlotting WesternIκB kinaseBiologyddc:616.07Myelin assemblyMicroglia/cytology/metabolismNerve Regeneration/physiologyDemyelinating Diseases/chemically induced/metabolism03 medical and health sciencesMyelinCuprizoneMice0302 clinical medicineCentral Nervous System/cytology/metabolismmedicineAnimalsRemyelinationCHUKMyelin Sheath030304 developmental biologyAstrocytes/cytology/metabolismMyelin Sheath/metabolism0303 health sciencesReverse Transcriptase Polymerase Chain ReactionSignal Transduction/physiologyI-Kappa-B KinaseNF-kappa BI-kappa B Kinase/metabolismOriginal ArticlesOligodendrocyte3. Good healthCell biologyI-kappa B KinaseNerve RegenerationOligodendrogliamedicine.anatomical_structureOligodendroglia/metabolismAstrocytesNF-kappa B/metabolismNeurogliaNeurology (clinical)MicrogliaNeuroscience030217 neurology & neurosurgeryDemyelinating DiseasesSignal Transduction
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Impact of a Three Amino Acid Deletion in the CH2 Domain of Murine IgG1 on Fc-Associated Effector Functions

2008

Abstract Four murine IgG subclasses display markedly different Fc-associated effector functions because of their differential binding to three activating IgG Fc receptors (FcγRI, FcγRIII, and FcγRIV) and C1q. Previous analysis of IgG subclass switch variants of 34-3C anti-RBC monoclonal autoantibodies revealed that the IgG1 subclass, which binds only to FcγRIII and fails to activate complement, displayed the poorest pathogenic potential. This could be related to the presence of a three amino acid deletion at positions 233–235 in the CH2 domain uniquely found in this subclass. To address this question, IgG1 insertion and IgG2b deletion mutants at positions 233–235 of 34-3C anti-RBC Abs were …

Deletion mutantImmunologyAntibody AffinityDown-Regulationddc:616.07BiologySubclassProtein Structure Tertiary/geneticsMiceAnimalsImmunology and AllergyAmino AcidsEffector functionsSequence DeletionMice Knockoutchemistry.chemical_classificationMice Inbred BALB CMice Inbred NZBAnemia Hemolytic Autoimmune/genetics/immunologyReceptors IgGAutoantibodyAmino Acids/chemistry/genetics/metabolismIgg subclassesReceptors IgG/antagonists & inhibitors/genetics/metabolismPathogenicityProtein Structure TertiaryImmunoglobulin G/genetics/metabolismImmunoglobulin Switch RegionCell biologyAmino acidImmunoglobulin Heavy Chains/biosynthesis/genetics/metabolismAntibody Affinity/geneticsBiochemistrychemistryImmunoglobulin GMonoclonalMutagenesis Site-DirectedAnemia Hemolytic AutoimmuneDown-Regulation/genetics/immunologyImmunoglobulin Heavy ChainsThe Journal of Immunology
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Crucial role of aspartic acid at position 265 in the CH2 domain for murine IgG2a and IgG2b Fc-associated effector functions.

2008

Abstract Replacement of aspartic acid by alanine at position 265 (D265A) in mouse IgG1 results in a complete loss of interaction between this isotype and low-affinity IgG Fc receptors (FcγRIIB and FcγRIII). However, it has not yet been defined whether the D265A substitution could exhibit similar effects on the interaction with two other FcγR (FcγRI and FcγRIV) and on the activation of complement. To address this question, 34-3C anti-RBC IgG2a and IgG2b switch variants bearing the D265A mutation were generated, and their effector functions and in vivo pathogenicity were compared with those of the respective wild-type Abs. The introduction of the D265A mutation almost completely abolished the…

ErythrocytesAspartic Acid/genetics/physiologyAntibodies Monoclonal/toxicityImmunologyMutantReceptors Fcddc:616.07Complement Activation/genetics/immunologyAlanine/geneticsMiceStructure-Activity RelationshipProtein structureImmunoglobulin G/chemistry/metabolismProtein Isoforms/chemistry/deficiency/genetics/physiologyAspartic acidImmunology and AllergyAnimalsProtein IsoformsErythrocytes/immunologyReceptorComplement ActivationAutoantibodiesAlanineMice KnockoutAspartic AcidMice Inbred BALB CAlaninebiologyAnemia Hemolytic Autoimmune/genetics/immunologyAntibodies MonoclonalReceptors Fc/chemistry/deficiency/genetics/physiologyFragment crystallizable regionIsotypeAmino Acid Substitution/genetics/physiologySialic Acids/geneticsProtein Structure TertiaryMice Inbred C57BLBiochemistryAmino Acid SubstitutionImmunoglobulin Gbiology.proteinSialic AcidsAutoantibodies/toxicityAnemia Hemolytic AutoimmuneAntibodyProtein Structure Tertiary/genetics/physiologyJournal of immunology (Baltimore, Md. : 1950)
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Immunodetection of the microvillous cytoskeleton molecules villin and ezrin in the parasitophorous vacuole wall of Cryptosporidium parvum (Protozoa: …

1999

Microvilli - actin - villin - ezrin - Cryptosporidium parvum The sporozoites and merozoites of the Apicomplexan protozoan Cryptosporidium parvum (C. parvum) invade the apical side of enterocytes and induce the formation of a parasitophorous vacuole which stays in the brush border area and disturbs the distribution of microvilli. The vacuole is separated from the apical cytoplasm of the cell by an electron-dense layer of undetermined composition. In order to characterize the enterocyte cytoskeleton changes that occur during C. parvum invasion and development, we used both confocal immunofluorescence and immunoelectron microscopy to examine at the C.parvum-enterocyte interface the distributio…

Feces/microbiologyIntestines/parasitologyMicrofilament Proteins/ analysisVacuoleddc:616.07Actins/analysisRats Sprague-DawleyFecesMiceEzrinCarrier Proteins/ analysisCryptosporidium/ chemistry/pathogenicity/ultrastructureCytoskeletonMicroscopy ImmunoelectronCytoskeletonMice Inbred BALB CMicroscopy ConfocalbiologyMicrovilliMicrofilament ProteinsCytoskeleton/ chemistryGeneral MedicineCell biologyIntestinesCryptosporidium parvumFemaleVillinHistologyImmunoelectron microscopyVacuoles/ultrastructurePhosphoproteins/ analysisCryptosporidiummacromolecular substancesPathology and Forensic Medicineparasitic diseasesAnimalsApical cytoplasmActinCell Biologybiology.organism_classificationPhosphoproteinsActinsRatsMicrovilli/ chemistryCytoskeletal ProteinsMicroscopy ElectronVacuolesbiology.proteinCarrier ProteinsEuropean journal of cell biology
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