Search results for "IMMUNOLOGY"

showing 10 items of 9651 documents

Ruling out nosocomial transmission of Cryptosporidium in a renal transplantation unit: case report

2016

Background Cryptosporidium spp. is a ubiquitous parasite affecting humans as well as domestic and wild vertebrates, causing diarrhea in both immunocompetent and immunocompromised hosts worldwide. Its transmission occurs primarily by the fecal-oral route. In humans, C. parvum and C. hominis are the most prevalent species, whereas immunocompetent and immunocompromised individuals can also be infected by other zoonotic species. Renal transplant patients are prone to develop cryptosporidiosis, which can induce severe and life-threatening diarrhea. Case presentation We report here a series of nearly concomitant cases of acute symptomatic cryptosporidiosis in three renal transplant patients atten…

0301 basic medicineNephrologyAdultDiarrheaMalemedicine.medical_specialty[SDV]Life Sciences [q-bio]030106 microbiologyCryptosporidiosisCryptosporidiumContext (language use)Case Report03 medical and health sciencesFecesImmunocompromised HostInternal medicinemedicineAnimalsHumans[SDV.MP.PAR]Life Sciences [q-bio]/Microbiology and Parasitology/ParasitologyGenotypingCross InfectionbiologyTransmission (medicine)NitazoxanideCryptosporidiumAcute Kidney InjuryMiddle Agedbiology.organism_classificationNitro CompoundsKidney Transplantation3. Good healthTransplantationDiarrheaThiazoles030104 developmental biologyInfectious DiseasesRenal transplant[SDV.MP]Life Sciences [q-bio]/Microbiology and ParasitologyImmunologyCoccidiostatsFemalemedicine.symptomZoonotic speciesmedicine.drugGenotypic species identification
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Genetic regulation and function of epidermal growth factor receptor signalling in patterning of the embryonicDrosophilabrain

2016

The specification of distinct neural cell types in central nervous system development crucially depends on positional cues conferred to neural stem cells in the neuroectoderm. Here, we investigate the regulation and function of the epidermal growth factor receptor (EGFR) signalling pathway in early development of theDrosophilabrain. We find that localized EGFR signalling in the brain neuroectoderm relies on a neuromere-specific deployment of activating (Spitz, Vein) and inhibiting (Argos) ligands. Activated EGFR controls the spatially restricted expression of all dorsoventral (DV) patterning genes in a gene- and neuromere-specific manner. Further, we reveal a novel role of DV genes—ventral …

0301 basic medicineNervous system197brain neuroblastsrhomboidBasic Helix-Loop-Helix Transcription FactorsDrosophila ProteinsEpidermal growth factor receptorPhosphorylationlcsh:QH301-705.5NeuregulinsNeural PlateGeneral NeuroscienceNeurogenesisBrainGene Expression Regulation DevelopmentalNuclear ProteinsAnatomyargosNeural stem cellHedgehog signaling pathwayCell biologyErbB ReceptorsDrosophila melanogastermedicine.anatomical_structureResearch ArticleSignal Transduction1001NeurogenesisImmunologyNerve Tissue ProteinsBiology133General Biochemistry Genetics and Molecular Biology03 medical and health sciencesNeuroblastveindorsoventral patterning genesmedicineAnimalsEye ProteinsReceptors Invertebrate PeptideBody PatterningHomeodomain ProteinsEpidermal Growth FactorNeuroectodermResearchMembrane Proteins58Embryonic stem cell030104 developmental biologylcsh:Biology (General)biology.proteinepidermal growth factor receptorTranscription FactorsOpen Biology
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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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Cholinergic signaling controls immune functions and promotes homeostasis

2020

Abstract Acetylcholine (ACh) was created by nature as one of the first signaling molecules, expressed already in procaryotes. Based on the positively charged nitrogen, ACh could initially mediate signaling in the absence of receptors. When evolution established more and more complex organisms the new emerging organs systems, like the smooth and skeletal muscle systems, energy-generating systems, sexual reproductive system, immune system and the nervous system have further optimized the cholinergic signaling machinery. Thus, it is not surprising that ACh and the cholinergic system are expressed in the vast majority of cells. Consequently, multiple common interfaces exist, for example, betwee…

0301 basic medicineNervous systemCell signalingImmunologyCholinergic AgentsBiology03 medical and health sciences0302 clinical medicineImmune systemMemorymedicineAnimalsHomeostasisHumansImmunologic FactorsLearningImmunology and AllergyReceptorOrganismPharmacologyImmunity030104 developmental biologymedicine.anatomical_structureImmune System030220 oncology & carcinogenesisCholinergicNeuroscienceHomeostasisAcetylcholineSignal Transductionmedicine.drugInternational Immunopharmacology
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Septin/anillin filaments scaffold central nervous system myelin to accelerate nerve conduction

2016

Myelination of axons facilitates rapid impulse propagation in the nervous system. The axon/myelin-unit becomes impaired in myelin-related disorders and upon normal aging. However, the molecular cause of many pathological features, including the frequently observed myelin outfoldings, remained unknown. Using label-free quantitative proteomics, we find that the presence of myelin outfoldings correlates with a loss of cytoskeletal septins in myelin. Regulated by phosphatidylinositol-(4,5)-bisphosphate (PI(4,5)P2)-levels, myelin septins (SEPT2/SEPT4/SEPT7/SEPT8) and the PI(4,5)P2-adaptor anillin form previously unrecognized filaments that extend longitudinally along myelinated axons. By confoca…

0301 basic medicineNervous systemCentral Nervous SystemProteomicsScaffoldMouseProteomeNeural ConductionSeptinNerve Fibers MyelinatedMyelinGene Knockout TechniquesMiceContractile ProteinsAxonBiology (General)CytoskeletonMicroscopy ImmunoelectronCytoskeletonMyelin SheathMicroscopy ConfocalGeneral NeuroscienceQRGeneral MedicineAnatomyCell biologyglial cellsmedicine.anatomical_structureGene TargetingMedicineResearch ArticleQH301-705.5ScienceCentral nervous systemmyelinated axonsmacromolecular substancesBiologyGeneral Biochemistry Genetics and Molecular Biologymyelin structure03 medical and health sciencesSeptin/anillin filaments; central nervous system; myelinlabel-free proteomicsmedicineAnimalsneuropathologyGeneral Immunology and Microbiology030104 developmental biologynervous systemseptin cytoskeletonProtein MultimerizationSeptinsSeptin cytoskeletonNeuroscienceeLife
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Influence of Commensal Microbiota on the Enteric Nervous System and Its Role in Neurodegenerative Diseases

2017

When thinking about neurodegenerative diseases, the first symptoms that come to mind are loss of memory and learning capabilities, which all resemble hallmarks of manifestation of such diseases in the central nervous system (CNS). However, the gut comprises the largest nervous system outside the CNS that is autonomously active and in close interplay with its microbiota. Therefore, the enteric nervous system (ENS) might serve as an indicator of degenerative pathomechanisms that also affect the CNS. On the other hand, it might offer an entry point for devastating influences from the microbial community or – conversely – for therapeutic approaches via gut commensals. Within the last years, the…

0301 basic medicineNervous systemGastrointestinal DiseasesCentral nervous systemNeurodegenerative DiseasesParkinson DiseaseFecal Microbiota TransplantationBiologyGut florabiology.organism_classificationEnteric Nervous SystemGastrointestinal Microbiome03 medical and health sciencesNeuroprotective Agents030104 developmental biology0302 clinical medicinemedicine.anatomical_structureAlzheimer DiseasemedicineAnimalsHumansImmunology and AllergyEnteric nervous systemNeuroscience030217 neurology & neurosurgeryJournal of Innate Immunity
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New Functions of APC/C Ubiquitin Ligase in the Nervous System and Its Role in Alzheimer’s Disease

2017

The E3 ubiquitin ligase Anaphase Promoting Complex/Cyclosome (APC/C) regulates important processes in cells, such as the cell cycle, by targeting a set of substrates for degradation. In the last decade, APC/C has been related to several major functions in the nervous system, including axon guidance, synaptic plasticity, neurogenesis, and neuronal survival. Interestingly, some of the identified APC/C substrates have been related to neurodegenerative diseases. There is an accumulation of some degradation targets of APC/C in Alzheimer’s disease (AD) brains, which suggests a dysregulation of the protein complex in the disorder. Moreover, recently evidence has been provided for an inactivation o…

0301 basic medicineNervous systemNeurogenesisUbiquitin-Protein LigasesReviewubiquitin ligaseNervous SystemCatalysisAnaphase-Promoting Complex-CyclosomeCdh1 ProteinsInorganic Chemistrylcsh:Chemistry03 medical and health sciencesMiceAlzheimer Diseasemedicineoxidative stressAnimalsHumansPhysical and Theoretical ChemistryMolecular Biologylcsh:QH301-705.5SpectroscopyNeuronsNeuronal PlasticitybiologyOrganic ChemistryNeurodegenerationNeurogenesisCell CycleneurodegenerationGeneral MedicineCell cyclemedicine.diseaseComputer Science ApplicationsUbiquitin ligaseCell biology030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)lcsh:QD1-999ImmunologyKnockout mouseProteolysisbiology.proteinAxon guidanceAnaphase-promoting complexexcitotoxicityInternational Journal of Molecular Sciences
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Fetal neurogenesis: breathe HIF you can.

2016

Blood vessels are part of the stem cell niche in the developing cerebral cortex, but their in vivo role in controlling the expansion and differentiation of neural stem cells (NSCs) in development has not been studied. Here, we report that relief of hypoxia in the developing cerebral cortex by ingrowth of blood vessels temporo‐spatially coincided with NSC differentiation. Selective perturbation of brain angiogenesis in vessel‐specific Gpr124 null embryos, which prevented the relief from hypoxia, increased NSC expansion at the expense of differentiation. Conversely, exposure to increased oxygen levels rescued NSC differentiation in Gpr124 null embryos and increased it further in WT embryos, s…

0301 basic medicineNeurogenesisNicheNeovascularization PhysiologicBiologyCell fate determinationGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesMiceFetusNeural Stem CellsmedicineAnimalsHumansNews & ViewsHypoxiaMolecular BiologyCentral elementreproductive and urinary physiologyCell ProliferationCerebral CortexFetusGeneral Immunology and MicrobiologyGeneral NeuroscienceNeurogenesisCell DifferentiationArticlesHypoxia-Inducible Factor 1 alpha Subunitnervous system diseasesOxygen030104 developmental biologymedicine.anatomical_structurenervous systemCerebral cortexImmunologyNeuronStem cellbiological phenomena cell phenomena and immunityNeuroscienceGlycolysisThe EMBO journal
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Pathogenesis of antiphospholipid syndrome: recent insights and emerging concepts

2018

Introduction: Even though our understanding of the antiphospholipid syndrome (APS) has improved tremendously over the last decades, we are still not in a position to replace symptomatic anticoagulation by pathogenesis based causal treatments. Areas covered: Recent years have provided further insights into pathogenetically relevant mechanisms. These include a differentiation of pathogenic subtypes of antiphospholipid antibodies (aPL), novel mechanisms modulating disease activity, for example, extracellular vesicles and microRNA, and novel players in pathogenesis, for example, neutrophils and neutrophil extracellular traps (NETs). Expert commentary: It is evident that aPL induce a proinflamma…

0301 basic medicineNeutrophilsImmunologyBioinformaticsExtracellular TrapsExtracellular vesiclesProinflammatory cytokinePathogenesisExtracellular VesiclesGenetic Heterogeneity03 medical and health sciences0302 clinical medicineimmune system diseasesAntiphospholipid syndromemicroRNAHumansImmunology and AllergyMedicineFetal lossBlood CoagulationComplement Activation030203 arthritis & rheumatologybusiness.industryNeutrophil extracellular trapsAntiphospholipid Syndromemedicine.diseaseMicroRNAs030104 developmental biologyAntibodies AntiphospholipidSignal transductionbusinessExpert Review of Clinical Immunology
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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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