Search results for "Mod"

showing 10 items of 39605 documents

Alterations in reelin and reelin receptors in Down syndrome.

2019

Reelin is an extracellular matrix glycoprotein that modulates synaptic function and plasticity, with a crucial role in neuronal migration. Changes in the expression of this protein have been reported in neurodegenerative diseases, such as Alzheimer's disease (AD). This molecule is produced by Cajal-Retzius neurons during development and by inhibitory neurons in the adult nervous system. Individuals with Down syndrome (DS) present an early development of AD; therefore, we analyzed the alterations in this molecule and its receptors in the murine model for DS Ts65Dn as well as in human with DS. We performed immunofluorescence analysis for reelin and its receptors very-low-density lipoprotein r…

0301 basic medicineNervous systemAdultMaleReceptor expressionCell Adhesion Molecules NeuronalNerve Tissue ProteinsReceptors Cell SurfaceTissue BanksInhibitory postsynaptic potential03 medical and health sciencesMice0302 clinical medicinemedicineAnimalsHumansReelinReceptorLDL-Receptor Related ProteinsAgedTemporal cortexNeuronsExtracellular Matrix ProteinsbiologyCell adhesion moleculeGeneral NeuroscienceSerine EndopeptidasesMiddle AgedTemporal LobeCell biologyDisease Models AnimalReelin Protein030104 developmental biologymedicine.anatomical_structurenervous systemReceptors LDLbiology.proteinDown Syndrome030217 neurology & neurosurgeryLipoproteinNeuroreport
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Two different pathogenic mechanisms, dying-back axonal neuropathy and pancreatic senescence, are present in the YG8R mouse model of Friedreich ataxia

2016

Frataxin (FXN) deficiency causes Friedreich's ataxia (FRDA), a multisystem disorder with neurological and non-neurological symptoms. FRDA pathophysiology combines developmental and degenerative processes of dorsal root ganglia (DRG), sensory nerves, dorsal columns and other central nervous structures. A dying-back mechanism has been proposed to explain the peripheral neuropathy and neuropathology. In addition, affected individuals have non-neuronal symptoms such as diabetes mellitus or glucose intolerance. To go further in the understanding of the pathogenic mechanisms of neuropathy and diabetes associated with the disease, we have investigated the humanized mouse YG8R model of FRDA. By bio…

0301 basic medicineNervous systemAgingPathologylcsh:MedicineMedicine (miscellaneous)Mice0302 clinical medicineImmunology and Microbiology (miscellaneous)Ganglia SpinalInsulin-Secreting CellsInsulin SecretionInsulinMuscle spindleDorsal root gangliaCellular SenescenceDiabetisbiologyMusclesDiabetesAnatomyMitochondria3. Good healthmedicine.anatomical_structureSistema nerviós simpàticDying-back neuropathyPeripheral nervous systemCell senescencemedicine.symptomOxidation-Reductionlcsh:RB1-214Research ArticleSenescencemedicine.medical_specialtyAtaxiaNeuroscience (miscellaneous)Friedreich’s ataxiaNeuropathologyGeneral Biochemistry Genetics and Molecular BiologyPàncreesMalalties del sistema nerviós03 medical and health sciencesPeripheral Nervous Systemlcsh:PathologymedicineAnimalsHumansPancreasIslet of Langerhanslcsh:R302Friedreich's ataxiaNervous system Diseasesmedicine.diseaseAxonsMice Inbred C57BLDisease Models Animal030104 developmental biologyPeripheral neuropathyFriedreich AtaxiaSympathetic nervous systemMutationHumanized mouseFrataxinbiology.proteinEnergy Metabolism030217 neurology & neurosurgeryDisease Models & Mechanisms
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Impairment of learning and memory performances induced by BPA Evidences from the literature of a MoA mediated through an ED

2018

International audience; Many rodent studies and a few non-human primate data report impairments of spatial and non-spatial memory induced by exposure to bisphenol A (BPA), which are associated with neural modifications, particularly in processes involved in synaptic plasticity. BPA-induced alterations involve disruption of the estrogenic pathway as established by reversal of BPA-induced effects with estrogenic receptor antagonist or by interference of BPA with administered estradiol in ovariectomized animals. Sex differences in hormonal impregnation during critical periods of development and their influence on maturation of learning and memory processes may explain the sexual dimorphism obs…

0301 basic medicineNervous systemNervous systemendocrine systemmedicine.drug_classEndocrine disruptionBiologyEndocrine DisruptorsBiochemistryLearning and memory03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEndocrinologyMESH: PhenolsBisphenol APhenolsMemorymedicineMESH: Benzhydryl CompoundsAnimalsHumansBenzhydryl compoundsMESH: MemoryBenzhydryl CompoundsMode of actionMolecular BiologyBehavior Animalurogenital systemBrainCognitionEnvironmental exposureEnvironmental ExposureReceptor antagonistMESH: Endocrine Disruptors030104 developmental biologymedicine.anatomical_structurechemistrySynaptic plasticity[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologieSignal transductionNeuroscience030217 neurology & neurosurgeryhormones hormone substitutes and hormone antagonists
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NO Hemodynamic Speed Limit for Hippocampal Neurogenesis

2019

Newborn dentate granule cells (DGCs) are continuously generated in the adult brain. The mechanism underlying how the adult brain governs hippocampal neurogenesis remains poorly understood. In this study, we investigated how coupling of pre-existing neurons to the cerebrovascular system regulates hippocampal neurogenesis. Using a new in vivo imaging method in freely moving mice, we found that hippocampus-engaged behaviors, such as exploration in a novel environment, rapidly increased microvascular blood flow velocity in the dentate gyrus. Importantly, blocking this exploration-elevated blood flow dampened experience-induced hippocampal neurogenesis. By imaging the neurovascular niche in comb…

0301 basic medicineNeurogenesisGeneral NeuroscienceNeurogenesisHemodynamicsHemodynamicsHippocampal formationBiologyHippocampusArticleCoupling (electronics)03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structurenervous systemNeuroblastVascular flowDentate GyrusmedicineNeurovascular CouplingNeuronNeuroscience030217 neurology & neurosurgeryNeuron
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Intrinsic volatility of synaptic connections — a challenge to the synaptic trace theory of memory

2017

According to the synaptic trace theory of memory, activity-induced changes in the pattern of synaptic connections underlie the storage of information for long periods. In this framework, the stability of memory critically depends on the stability of the underlying synaptic connections. Surprisingly however, synaptic connections in the living brain are highly volatile, which poses a fundamental challenge to the synaptic trace theory. Here we review recent experimental evidence that link the initial formation of a memory with changes in the pattern of connectivity, but also evidence that synaptic connections are considerably volatile even in the absence of learning. Then we consider different…

0301 basic medicineNeuronal PlasticityGeneral Neuroscience[SCCO.NEUR]Cognitive science/NeuroscienceModels NeurologicalTheoretical modelsBrain03 medical and health sciences030104 developmental biology0302 clinical medicineAnti-Hebbian learningMemoryNeuroplasticityMetaplasticityNeural PathwaysSynapsesAnimalsHumansLearningPsychologyNeuroscience030217 neurology & neurosurgeryComputingMilieux_MISCELLANEOUSTrace theory
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A stable brain from unstable components: Emerging concepts and implications for neural computation.

2017

Neuroscientists have often described the adult brain in similar terms to an electronic circuit board- dependent on fixed, precise connectivity. However, with the advent of technologies allowing chronic measurements of neural structure and function, the emerging picture is that neural networks undergo significant remodeling over multiple timescales, even in the absence of experimenter-induced learning or sensory perturbation. Here, we attempt to reconcile the parallel observations that critical brain functions are stably maintained, while synapse- and single-cell properties appear to be reformatted regularly throughout adult life. In this review, we discuss experimental evidence at multiple …

0301 basic medicineNeuronsArtificial neural networkGeneral NeuroscienceComputationModels NeurologicalBrainSensory systemSynapse03 medical and health sciences030104 developmental biology0302 clinical medicineModels of neural computationBiological neural networkAnimalsHumansNeural Networks ComputerPsychologyNeuroscience030217 neurology & neurosurgeryDynamic equilibriumElectronic circuitNeuroscience
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Neutrophil extracellular traps impair fungal clearance in a mouse model of invasive pulmonary aspergillosis

2019

Abstract Neutrophil extracellular traps (NETs) are formed by polymorphonuclear neutrophils (PMN) and contribute to the innate host defense by binding and killing bacterial and fungal pathogens. Because NET formation depends on histone hypercitrullination by peptidylarginine deiminase 4 (PAD4), we used PAD4 gene deficient (Pad4-/-) mice in a mouse model of invasive pulmonary aspergillosis (IPA) to address the contribution of NETs to the innate host defense in vivo. After the induction (24 h) of IPA by i.t. infection with Aspergillus fumigatus conidia, Pad4-/- mice revealed lower fungal burden in the lungs, accompanied by less acute lung injury, TNFα and citH3 compared to wildtype controls. T…

0301 basic medicineNeutrophilsImmunologyMedizinApoptosisLung injuryExtracellular TrapsArticleAspergillus fumigatusMicrobiologyMice03 medical and health sciences0302 clinical medicineProtein-Arginine Deiminase Type 4In vivomedicineAnimalsHumansImmunology and Allergyskin and connective tissue diseasesLungInvasive Pulmonary AspergillosisMice KnockoutLungbiologyAspergillus fumigatusWild typeHematologyNeutrophil extracellular trapsbiology.organism_classificationmedicine.diseaseImmunity Innaterespiratory tract diseasesMice Inbred C57BLDisease Models AnimalPneumonia030104 developmental biologymedicine.anatomical_structureCitrullinationTumor necrosis factor alpha030215 immunologyImmunobiology
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Parasite Clearance in Leishmaniasis in Resistant Animals Is Independent of the IL-23/IL-17A Axis

2015

0301 basic medicineNeutrophilsLeishmaniasis CutaneousDermatologyBiologyBiochemistryMice03 medical and health sciences0302 clinical medicineInterleukin 23medicineAnimalsParasite hostingGenetic Predisposition to DiseaseMolecular BiologyLeishmania majorMice KnockoutInterleukin-17LeishmaniasisCell Biologymedicine.diseaseMice Inbred C57BLDisease Models Animal030104 developmental biologyImmunologyInterleukin-23 Subunit p19Th17 CellsFemale030215 immunologyJournal of Investigative Dermatology
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Regulatory T Cells Prevent Neutrophilic Infiltration of Skin during Contact Hypersensitivity Reactions by Strengthening the Endothelial Barrier

2020

The healing phase of contact hypersensitivity reactions is critically dependent on regulatory T cells (Tregs), but even the early inflammatory phase, that is, 6-24 hours after induction of a contact hypersensitivity reaction, is susceptible to Treg-mediated suppression. To investigate the underlying mechanisms, we injected Tregs before the challenge and analyzed the skin-infiltrating cells as early as 6 hours later. Early on, we found mainly neutrophils in the challenged skin, but only a few T cells. This influx of neutrophils was blocked by the injection of Tregs, indicating that they were able to prevent the first wave of leukocytes, which are responsible for starting an immune reaction. …

0301 basic medicineNeutrophilsRegulatory T cellchemical and pharmacologic phenomenaCell CommunicationPicryl ChlorideDermatologyFilaminT-Lymphocytes RegulatoryBiochemistryProinflammatory cytokineMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationNectinmedicineAnimalsHumansProtein kinase AMolecular BiologySkinChemistryChemotaxisCell BiologyCell biologyEndothelial stem cellDisease Models Animal030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisDermatitis Allergic ContactEndothelium VascularIntracellularJournal of Investigative Dermatology
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Chemistry, Pharmacodynamics, and Pharmacokinetics of NSAIDs

2016

Numerous chemically different entities are clustered under the label of nonsteroidal anti-inflammatory drugs (NSAIDs). They share the ability to inhibit prostanoid synthesis by blocking the activity of the cyclooxygenase enzymes and, as a consequence, to exert anti-inflammatory, analgesic, and antipyretic effects. On the other hand, by hindering the housekeeping roles of prostaglandins, they also deteriorate the gastrointestinal mucosal barrier and the renal and endothelial hemodynamic regulation. The present chapter compiles available pharmacokinetic and pharmacodynamic data that may help to understand the different therapeutic profiles reported for particular agents.

0301 basic medicineNonsteroidalbiologyChemistryAnalgesicHemodynamic regulation030204 cardiovascular system & hematologyPharmacologyProstanoid synthesis03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicinePharmacokineticsPharmacodynamicsbiology.proteinmedicineCyclooxygenaseAntipyreticmedicine.drug
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