Search results for "Cause"

showing 10 items of 6525 documents

The therapeutic potential of inorganic polyphosphate: A versatile physiological polymer to control coronavirus disease (COVID-19).

2021

Rationale: The pandemic caused by the novel coronavirus SARS-CoV-2 is advancing rapidly. In particular, the number of severe courses of the disease is still dramatically high. An efficient drug therapy that helps to improve significantly the fatal combination of damages in the airway epithelia, in the extensive pulmonary microvascularization and finally multiorgan failure, is missing. The physiological, inorganic polymer, polyphosphate (polyP) is a molecule which could prevent the initial phase of the virus life cycle, the attachment of the virus to the target cells, and improve the epithelial integrity as well as the mucus barrier. Results: Surprisingly, polyP matches perfectly with the ca…

0301 basic medicineDrug Evaluation PreclinicalMedicine (miscellaneous)Virus AttachmentRespiratory MucosaReviewmedicine.disease_causeAntiviral Agents03 medical and health sciencesMice0302 clinical medicinePolyphosphatesmedicineAnimalsHumansMode of actionReceptorPharmacology Toxicology and Pharmaceutics (miscellaneous)PandemicsMUC1Coronaviruschemistry.chemical_classificationChemistrySARS-CoV-2MucinMucinsCOVID-19Epithelial CellspolyphosphateMucusdigestive system diseasesCell biologyCOVID-19 Drug TreatmentDisease Models Animal030104 developmental biology030220 oncology & carcinogenesisAlkaline phosphataseNanoparticlesGlycoproteinviral receptor-binding domainTheranostics
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Exercise training as a drug to treat age associated frailty

2016

Exercise causes an increase in the production of free radicals [1]. As a result of a hormetic mechanism antioxidant enzymes are synthesised and the cells are protected against further oxidative stress. Thus, exercise can be considered as an antioxidant [2]. Age-associated frailty is a major medical and social concern as it can easily lead to dependency. In this review we describe that oxidative stress is associated with frailty and the mechanism by which exercise prevents age-associated frailty. We propose that individually tailored multicomponent exercise programmes are one of the best ways to prevent and to treat age-associated frailty.

0301 basic medicineDrugGerontologyAgingmedicine.medical_specialtyRos signallingFree Radicalsmedia_common.quotation_subjectmedicine.disease_causeBiochemistry03 medical and health sciencesPhysiology (medical)HumansMedicineIntensive care medicineExercisemedia_commonFrailtybusiness.industryMechanism (biology)TOR Serine-Threonine KinasesHormesisMitochondriaOxidative Stress030104 developmental biologybusinessOxidative stressFree Radical Biology and Medicine
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Beneficial Role of Exercise in the Modulation of

2021

Duchenne muscular dystrophy (DMD) is an X-linked recessive progressive lethal disorder caused by the lack of dystrophin, which determines myofibers mechanical instability, oxidative stress, inflammation, and susceptibility to contraction-induced injuries. Unfortunately, at present, there is no efficient therapy for DMD. Beyond several promising gene- and stem cells-based strategies under investigation, physical activity may represent a valid noninvasive therapeutic approach to slow down the progression of the pathology. However, ethical issues, the limited number of studies in humans and the lack of consistency of the investigated training interventions generate loss of consensus regarding …

0301 basic medicineDuchenne muscular dystrophyPhysiologyDuchenne muscular dystrophyClinical BiochemistryInflammationReviewBioinformaticsmedicine.disease_causeBiochemistrySettore BIO/09 - FisiologiaMuscle hypertrophy03 medical and health sciencesTherapeutic approach0302 clinical medicineFibrosismedicineTrainingMuscle inflammationVoluntary exerciseMolecular BiologySwimmingbiologybusiness.industrylcsh:RM1-950ROSCell Biologymedicine.diseaselcsh:Therapeutics. Pharmacology030104 developmental biologyantioxidantsTreadmill runningbiology.proteinmedicine.symptomAntioxidantDystrophinExercise prescriptionbusiness030217 neurology & neurosurgeryOxidative stressAntioxidants (Basel, Switzerland)
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A Novel Open and Infectious Form of Echovirus 1.

2016

ABSTRACT One of the hallmarks of enterovirus genome delivery is the formation of an uncoating intermediate particle. Based on previous studies of mostly heated picornavirus particles, intermediate particles were shown to have externalized the innermost capsid protein (VP4) and exposed the N terminus of VP1 and to have reduced infectivity. Here, in addition to the native and intact particle type, we have identified another type of infectious echovirus 1 (E1) particle population during infection. Our results show that E1 is slightly altered during entry, which leads to the broadening of the major virion peak in the sucrose gradient. In contrast, CsCl gradient separation revealed that in addit…

0301 basic medicineEchovirusPicornavirusvirusesImmunologyPopulationmedicine.disease_causeMicrobiology03 medical and health sciencesVirologymedicineEnterovirus InfectionsHumansgenome deliveryeducationInfectivityeducation.field_of_studybiologyVirionRNAbiology.organism_classificationVirologyEnterovirus B HumanVirus-Cell Interactionsenterovirukset030104 developmental biologyCapsidInsect Scienceintermediate particlesBiophysicsParticleRNA ViralCapsid ProteinsEchovirus 1Binding domainJournal of virology
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Sema3a plays a role in the pathogenesis of CHARGE syndrome

2018

CHARGE syndrome is an autosomal dominant malformation disorder caused by heterozygous loss of function mutations in the chromatin remodeler CHD7. Chd7 regulates the expression of Sema3a, which also contributes to the pathogenesis of Kallmann syndrome, a heterogeneous condition with the typical features hypogonadotropic hypogonadism and an impaired sense of smell. Both features are common in CHARGE syndrome suggesting that SEMA3A may provide a genetic link between these syndromes. Indeed, we find evidence that SEMA3A plays a role in the pathogenesis of CHARGE syndrome. First, Chd7 is enriched at the Sema3a promotor in neural crest cells and loss of function of Chd7 inhibits Sema3a expression…

0301 basic medicineEmbryo NonmammalianKallmann syndromePHENOTYPIC SPECTRUMmedicine.disease_causeSeverity of Illness IndexEpigenesis GeneticPathogenesisAXON GUIDANCECHD7CHARGE syndromeXenopus laevis0302 clinical medicineHYPOGONADOTROPIC HYPOGONADISMPromoter Regions GeneticGenetics (clinical)GeneticsMutationGeneral MedicinePhenotypeDNA-Binding ProteinsNEURAL CREST CELLSNeural CrestHomeobox Protein Nkx-2.5MIGRATIONBiology03 medical and health sciencesHypogonadotropic hypogonadismKALLMANN-SYNDROMEGeneticsmedicineAnimalsHumansEpigeneticsSHORT STATUREMolecular BiologyLoss functionMUTATIONSGenetic Complementation TestDNA HelicasesSemaphorin-3AKallmann Syndromemedicine.diseaseDisease Models Animal030104 developmental biologyHEK293 CellsXENOPUS-EMBRYOSMutationCHARGE Syndrome030217 neurology & neurosurgery
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Coexposure to sulfamethoxazole and cadmium impairs development and attenuates transcriptional response in sea urchin embryo

2017

Abstract Among sulfonamides, sulfamethoxazole represents one of the most widely employed. A considerable amount of sulfamethoxazole is introduced into the marine environment after utilization in aquaculture. The cytotoxicity of sulfamethoxazole relies mainly on arylhydroxylamine metabolites and it is associated with the production of reactive oxygen species. Cadmium represents a metal largely employed in several anthropic activities and it is toxic for all living organisms even at low concentrations. Since it is not degraded, cadmium irreversibly accumulates into cells. In order to understand the mechanisms of response to changes in the chemical environment, we investigated by light microsc…

0301 basic medicineEmbryo NonmammalianSulfamethoxazoleHealth Toxicology and Mutagenesis; Defense mechanisms;Gene ExpressionAquaculture010501 environmental sciencesmedicine.disease_cause01 natural sciencesCoexposureToxicologychemistry.chemical_compoundCadmium ChlorideGene expression profile; Stress responsechemistry.chemical_classificationCadmiumeducation.field_of_studyEchinodermSulfamethoxazoleChemistry (all)General MedicinePollutionCadmiumDefense mechanismEchinodermsmedicine.drugProgrammed cell deathEnvironmental EngineeringPopulationchemistry.chemical_elementSettore BIO/11 - Biologia MolecolareCadmium chlorideBiologyMicrobiologyCoexposure; Defense mechanisms; Echinoderms; Gene expression profile; Stress response; Chemistry (all); Environmental Chemistry03 medical and health sciencesDetoxificationmedicineAnimalsEnvironmental Chemistryeducation0105 earth and related environmental sciencesReactive oxygen speciesStress responsePublic Health Environmental and Occupational HealthGeneral ChemistryGene expression profile030104 developmental biologychemistrySea UrchinsWater Pollutants ChemicalOxidative stress
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An Intronic cis-Regulatory Element Is Crucial for the Alpha Tubulin Pl-Tuba1a Gene Activation in the Ciliary Band and Animal Pole Neurogenic Domains …

2017

In sea urchin development, structures derived from neurogenic territory control the swimming and feeding responses of the pluteus as well as the process of metamorphosis. We have previously isolated an alpha tubulin family member of Paracentrotus lividus (Pl-Tuba1a, formerly known as Pl-Talpha2) that is specifically expressed in the ciliary band and animal pole neurogenic domains of the sea urchin embryo. In order to identify cis-regulatory elements controlling its spatio-temporal expression, we conducted gene transfer experiments, transgene deletions and site specific mutagenesis. Thus, a genomic region of about 2.6 Kb of Pl-Tuba1a, containing four Interspecifically Conserved Regions (ICRs…

0301 basic medicineEmbryologyPolarity in embryogenesislcsh:MedicineGene ExpressionMedicine (all); Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)medicine.disease_causeBiochemistryTubulinGene expressionElectron MicroscopyTransgeneslcsh:SciencePromoter Regions GeneticSea urchinConserved SequenceSequence DeletionGeneticsRegulation of gene expressionMicroscopyMutationMultidisciplinaryMedicine (all)Gene Expression Regulation DevelopmentalGenomicsAnimal ModelsTATA BoxEnzymesEnhancer Elements GeneticExperimental Organism Systemsembryonic structuresParacentrotusTranscription Initiation SiteOxidoreductasesLuciferaseResearch ArticleEchinodermsTranscriptional ActivationImaging TechniquesNeurogenesisGreen Fluorescent ProteinsEmbryonic DevelopmentSettore BIO/11 - Biologia MolecolareBiologyResearch and Analysis MethodsGenome ComplexityParacentrotus lividus03 medical and health sciencesSpecies SpecificityTubulinsbiology.animalFluorescence ImagingGeneticsmedicineConsensus sequenceAnimalsCiliaEnhancerBiochemistry Genetics and Molecular Biology (all)Binding SitesModels Geneticlcsh:REmbryosOrganismsBiology and Life SciencesComputational BiologyProteinsbiology.organism_classificationInvertebratesIntronsCytoskeletal Proteins030104 developmental biologyAgricultural and Biological Sciences (all)Bright Field ImagingSea UrchinsEnzymologyMutagenesis Site-Directedlcsh:QTransmission Electron MicroscopyDevelopmental BiologyTranscription FactorsPLOS ONE
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IL ‐1 signaling is critical for expansion but not generation of autoreactive GM ‐ CSF + Th17 cells

2016

Abstract Interleukin‐1 (IL‐1) is implicated in numerous pathologies, including multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). However, the exact mechanism by which IL‐1 is involved in the generation of pathogenic T cells and in disease development remains largely unknown. We found that following EAE induction, pertussis toxin administration leads to IL‐1 receptor type 1 (IL‐1R1)‐dependent IL‐1β expression by myeloid cells in the draining lymph nodes. This myeloid‐derived IL‐1β did not vitally contribute to the generation and plasticity of Th17 cells, but rather promoted the expansion of a GM‐CSF + Th17 cell subset, thereby enhancing its encephalitog…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalBiologymedicine.disease_causePertussis toxinGeneral Biochemistry Genetics and Molecular BiologyAutoimmunityMice03 medical and health sciences0302 clinical medicineMediatormedicineAnimalsInducerMolecular BiologyCell ProliferationGeneral Immunology and MicrobiologyGeneral NeuroscienceMultiple sclerosisExperimental autoimmune encephalomyelitisGranulocyte-Macrophage Colony-Stimulating FactorArticlesmedicine.diseaseCell biology030104 developmental biologyPertussis ToxinT cell subsetImmunologyTh17 CellsLymphInterleukin-1030215 immunologyThe EMBO Journal
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Targeting CD52 does not affect murine neuron and microglia function.

2020

The humanized anti-CD52 antibody alemtuzumab is successfully used in the treatment of multiple sclerosis (MS) and is thought to exert most of its therapeutic action by depletion and repopulation of mainly B and T lymphocytes. Although neuroprotective effects of alemtuzumab have been suggested, direct effects of anti-CD52 treatment on glial cells and neurons within the CNS itself have not been investigated so far. Here, we show CD52 expression in murine neurons, astrocytes and microglia, both in vitro and in vivo. As expected, anti CD52-treatment caused profound lymphopenia and improved disease symptoms in mice subjected to experimental autoimmune encephalomyelitis (EAE). CD52 blockade also …

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalCD52Excitotoxicitymedicine.disease_causeNeuroprotection03 medical and health sciencesMice0302 clinical medicinemedicineAnimalsAlemtuzumabPharmacologyNeuronsMicrogliabusiness.industryMultiple sclerosisExperimental autoimmune encephalomyelitismedicine.disease030104 developmental biologymedicine.anatomical_structureCD52 AntigenGene Expression RegulationAlemtuzumabCalciumNeuronMicrogliabusinessNeuroscience030217 neurology & neurosurgerymedicine.drugEuropean journal of pharmacology
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Dendritic cells tip the balance towards induction of regulatory T cells upon priming in experimental autoimmune encephalomyelitis

2016

Counter-balancing regulatory mechanisms, such as the induction of regulatory T cells (Treg), limit the effects of autoimmune attack in neuroinflammation. However, the role of dendritic cells (DCs) as the most powerful antigen-presenting cells, which are intriguing therapeutic targets in this context, is not fully understood. Here, we demonstrate that conditional ablation of DCs during the priming phase of myelin-specific T cells in experimental autoimmune encephalomyelitis (EAE) selectively aborts inducible Treg (iTreg) induction, whereas generation of T helper (Th)1/17 cells is unaltered. DCs facilitate iTreg induction by creating a milieu with high levels of interleukin (IL)-2 due to a st…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalImmunologyMedizinPriming (immunology)chemical and pharmacologic phenomenaAutoimmunitymedicine.disease_causeLymphocyte ActivationT-Lymphocytes RegulatoryAutoimmunityImmunomodulation03 medical and health sciencesMice0302 clinical medicineT-Lymphocyte SubsetsTransforming Growth Factor betamedicineImmunology and AllergyAnimalsNeuroinflammationCD40biologyMultiple sclerosisExperimental autoimmune encephalomyelitisInterleukinhemic and immune systemsDendritic Cellsmedicine.disease030104 developmental biologyImmunologybiology.proteinInterleukin 12CytokinesTh17 Cells030217 neurology & neurosurgery
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