Search results for " mouse"

showing 10 items of 343 documents

The helminth community of Apodemus sylvaticus (Rodentia, Muridae) in the Sierra de Gredos (Spain)

2004

The Spanish mountain range of Gredos was included in the studies conducted on the Iberian peninsula to investigate helminth fauna of small mammals. The helminth community of the wood mouse, Apodemus sylvaticus (Rodentia, Muridae), was analysed. Qualitatively, 13 helminth species were detected: Plagiorchis sp. I and Plagiorchis sp. II (Trematoda); Taenia parva larvae, T. martis larvae, T. taeniaeformis larvae, Rodentolepis straminea and R. fraterna (Cestoda); and Trichuris muris, Heligmosomoides polygyrus, Syphacia stroma, S. frederici, Aspiculuris tetraptera and Rictularia proni (Nematoda). Quantitatively, the highest prevalence (65.0%) and the mean abundance (36.9%) of H. polygyrus stand o…

Plagiorchisfood.ingredientbiologyEcologyFaunaCestodabiology.organism_classificationWood mousefoodApodemusHelminthsAnimal Science and ZoologyHeligmosomoides polygyrusMuridaeArxius de Miscel·lània Zoològica
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Compromised central tolerance of ICA69 induces multiple organ autoimmunity

2014

For reasons not fully understood, patients with an organ-specific autoimmune disease have increased risks of developing autoimmune responses against other organs/tissues. We identified ICA69, a known β-cell autoantigen in Type 1 diabetes, as a potential common target in multi-organ autoimmunity. NOD mice immunized with ICA69 polypeptides exhibited exacerbated inflammation not only in the islets, but also in the salivary glands. To further investigate ICA69 autoimmunity, two genetically modified mouse lines were generated to modulate thymic ICA69 expression: the heterozygous ICA69(del/wt) line and the thymic medullary epithelial cell-specific deletion Aire-ΔICA69 line. Suboptimal central neg…

Primary Sjogren's syndromeGenetically modified mouseImmunologyThyroid GlandAutoimmune diabeteMice TransgenicThymus GlandBiologymedicine.disease_causeAutoantigensArticleSalivary GlandsSettore MED/13 - EndocrinologiaAutoimmune DiseasesAutoimmunityImmune toleranceAutoimmune thyroiditisIslets of LangerhansMiceICA69Mice Inbred NODImmune TolerancemedicineAnimalsImmunology and AllergyThymuAutoimmune thyroiditiNOD miceInflammationAutoimmune diseaseStomachmedicine.diseaseGene Expression RegulationAutoimmune polyendocrine syndromeImmunologyAutoimmune polyendocrine syndromeCentral toleranceJournal of Autoimmunity
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Increased oxidative stress and impaired antioxidant response in Lafora disease.

2014

15 páginas, 10 figuras

ProteomicsGenetically modified mouseAntioxidantmedicine.medical_treatmentNeuroscience (miscellaneous)Proteomic analysisMice TransgenicBiologymedicine.disease_causeBiochemistryAntioxidantsLafora diseaseMiceCellular and Molecular NeuroscienceLaforinPhysiology (medical)AutophagymedicineAnimalsHumansLafora diseaseMice Knockoutchemistry.chemical_classificationReactive oxygen speciesAutophagymedicine.diseaseMalinCell biologyNeurologychemistryBiochemistryOxidative stressMutationAntioxidant enzymesReactive Oxygen SpeciesLaforinOxidative stressIntracellularFree radical biologymedicine
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Membrane vesicles containing matrix metalloproteinase-9 and fibroblast growth factor-2 are released into the extracellular space from mouse mesoangio…

2010

Certain proteins, including fibroblast growth factor-2 (FGF-2) and matrix metalloproteinase-9 (MMP-9), have proved very effective in increasing the efficacy of mesoangioblast stem cell therapy in repairing damaged tissue. We provide the first evidence that mouse mesoangioblast stem cells release FGF-2 and MMP-9 in their active form through the production of membrane vesicles. These vesicles are produced and turned over continuously, but are stable for some time in the extracellular milieu. Mesoangioblasts shed membrane vesicles even under oxygen tensions that are lower than those typically used for cell culture and more like those of mouse tissues. These findings suggest that mesoangioblast…

ProteomicsTime FactorsPhysiologyClinical BiochemistryBiologyFibroblast growth factorCell LineMiceMembrane MicrodomainsTubulinParacrine CommunicationmedicineExtracellularAnimalsSecretionSettore BIO/06 - Anatomia Comparata E CitologiaFibroblastCytoskeletonMembrane vesicles MMP9 FGF2 mouse mesoangioblastMesoangioblastSecretory VesiclesVesicleBiological TransportMesenchymal Stem CellsCell BiologyCell biologyOxygenmedicine.anatomical_structureMatrix Metalloproteinase 9Cell cultureFibroblast Growth Factor 2Stem cellExtracellular Space
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Head and Neck Cancers

2005

Pyriform SinusNude mousebiologybusiness.industryFalse Vocal CordTonsillar fossaMedicineAnatomyHead and neckbusinessbiology.organism_classification
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Amyloid Beta-Mediated Changes in Synaptic Function and Spine Number of Neocortical Neurons Depend on NMDA Receptors

2021

Onset and progression of Alzheimer’s disease (AD) pathophysiology differs between brain regions. The neocortex, for example, is a brain region that is affected very early during AD. NMDA receptors (NMDARs) are involved in mediating amyloid beta (Aβ) toxicity. NMDAR expression, on the other hand, can be affected by Aβ. We tested whether the high vulnerability of neocortical neurons for Aβ-toxicity may result from specific NMDAR expression profiles or from a particular regulation of NMDAR expression by Aβ. Electrophysiological analyses suggested that pyramidal cells of 6-months-old wildtype mice express mostly GluN1/GluN2A NMDARs. While synaptic NMDAR-mediated currents are unaltered in 5xFAD …

QH301-705.5Amyloid betasomatosensory cortexDendritic SpinesMice TransgenicNeocortexSomatosensory systemReceptors N-Methyl-D-AspartateCatalysisArticleInorganic ChemistryAlzheimer Diseasemental disordersmedicineAnimalsBiology (General)Physical and Theoretical ChemistryQD1-999Molecular BiologySpectroscopyNeuronsNeocortexAmyloid beta-PeptidesbiologyPyramidal Cellsmusculoskeletal neural and ocular physiologyOrganic ChemistryWild typeAmyloid betaExcitatory Postsynaptic PotentialsGeneral Medicine5xFADPathophysiologyComputer Science ApplicationsNMDARChemistryElectrophysiologyProtein Subunitsmedicine.anatomical_structurenervous systemKnockout mouseSynapsesbiology.proteinNMDA receptorbiological phenomena cell phenomena and immunityNeuroscienceAlzheimer’s diseasepsychological phenomena and processesInternational Journal of Molecular Sciences
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Age-dependent regulation of antioxidant genes by p38α MAPK in the liver

2018

p38α is a redox sensitive MAPK activated by pro-inflammatory cytokines and environmental, genotoxic and endoplasmic reticulum stresses. The aim of this work was to assess whether p38α controls the antioxidant defense in the liver, and if so, to elucidate the mechanism(s) involved and the age-related changes. For this purpose, we used liver-specific p38α-deficient mice at two different ages: young-mice (4 months-old) and old-mice (24 months-old). The liver of young p38α knock-out mice exhibited a decrease in GSH levels and an increase in GSSG/GSH ratio and malondialdehyde levels. However, old mice deficient in p38α had higher hepatic GSH levels and lower GSSG/GSH ratio than young p38α knock-…

ROS Reactive oxygen species;RSK1 Ribosomal S6 kinase10301 basic medicineMAPK/ERK pathwayAgingHPLC High-performance liquid chromatographyAntioxidantmedicine.medical_treatmentTBP TATA-binding proteinClinical BiochemistryDEN Diethyl nitrosamine;MKP-1 MAPK phosphatase-1IκB kinaseGCLc Glutamate cysteine ligase catalytic subunitp38 Mitogen-Activated Protein KinasesG6PDH Glucose-6-phosphate dehydrogenaseBiochemistryAntioxidantsMicechemistry.chemical_compoundSuperoxide Dismutase-1Akt Protein kinase B0302 clinical medicineNrf2 Nuclear factor erythroid 2-related factor-2IL InterleukinSOD1 Cu/Zn-superoxide dismutaselcsh:QH301-705.5Mice KnockoutMK2 MAP-activated protein kinase 2;PGC-1α Peroxisome proliferator-activated receptor gamma coactivator 1-alphachemistry.chemical_classificationlcsh:R5-920Trx ThioredoxinGlutathione DisulfideTNF-α Tumor necrosis factor-alphabiologyLPS Lipopolysaccharide;GSSG Oxidized glutathione;MEF Mouse embryonic fibroblastsNF-kappa BGstm1 Glutathione S-transferase mu 1CatalaseEndoplasmic Reticulum StressGlutathioneLiverGSH Reduced glutathione;Catalase030220 oncology & carcinogenesisJNK c-Jun N-terminal kinaselcsh:Medicine (General)Research Papermedicine.medical_specialtyNF-E2-Related Factor 2Glutamate-Cysteine LigaseMKK MAPK kinaseAP-1 Activator protein-1IKK IƙB KinaseGene Expression Regulation EnzymologicSuperoxide dismutase03 medical and health sciencesInternal medicineGlutamate cysteine ligaseEGFR Epidermal growth factor receptormedicineAnimalsNuclear factor ƙBAnd catalaseChIP Chromatin immunoprecipitation;Protein kinase BNF-ƙB Nuclear factor kappa BSuperoxide DismutaseSuperoxide dismutase 1Superoxide dismutase 2Organic ChemistryGlutathioneASK1 Apoptosis signal-regulating kinase 1ATF2 activating transcription factor 2;030104 developmental biologyEndocrinologyEnzymeHsp Heat shock proteinlcsh:Biology (General)chemistrybiology.proteinSOD2 Mn-superoxide dismutaseMAPK mitogen activated protein kinaseNEM N-ethyl maleimide;Redox Biology
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Inducible and reversible inhibition of miRNA-mediated gene repression in vivo

2021

Although virtually all gene networks are predicted to be controlled by miRNAs, the contribution of this important layer of gene regulation to tissue homeostasis in adult animals remains unclear. Gain and loss of function experiments have provided key insights into the specific function of individual miRNAs, but effective genetic tools to study the functional consequences of global inhibition of miRNA activity in vivo are lacking. Here we report the generation and characterization of a genetically engineered mouse strain in which miRNA-mediated gene repression can be reversibly inhibited without affecting miRNA biogenesis or abundance. We demonstrate the usefulness of this strategy by invest…

Regulation of gene expressionGenetically Engineered MouseRegeneration (biology)microRNAGene regulatory networkBiologyLoss functionFunction (biology)Tissue homeostasisCell biology
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2015

Transporters of the ATP-binding cassette (ABC) family such as MDR1 play a pivotal role in persistence of brain homeostasis by contributing to the strict permeability properties of the blood–brain barrier. This barrier on one hand compromises treatment of central nervous system diseases by restricting access of drugs; on the other hand, an impaired or altered function of barrier building cells has been described in neurological disorders. The latter might contribute to increased vulnerability of the brain under pathological conditions or even enforce pathogenesis. Here, we present a novel approach for a systematic examination of drug impact on Mdr1 gene expression by establishing a dual repo…

Reporter genebiologyPromoterPharmacologyBlood–brain barrierCell biologychemistry.chemical_compoundmedicine.anatomical_structureNeurologychemistryKnockout mouseGene expressionOltiprazbiology.proteinmedicineGeneral Pharmacology Toxicology and PharmaceuticsEnhancerP-glycoproteinPharmacology Research & Perspectives
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Impaired formation of the inner retina in an AChE knockout mouse results in degeneration of all photoreceptors

2004

Blinding diseases can be assigned predominantly to genetic defects of the photoreceptor/pigmented epithelium complex. As an alternative, we show here for an acetylcholinesterase (AChE) knockout mouse that photoreceptor degeneration follows an impaired development of the inner retina. During the first 15 postnatal days of the AChE-/- retina, three major calretinin sublaminae of the inner plexiform layer (IPL) are disturbed. Thereby, processes of amacrine and ganglion cells diffusely criss-cross throughout the IPL. In contrast, parvalbumin cells present a nonlaminar IPL pattern in the wild-type, but in the AChE-/- mouse their processes become structured within two 'novel' sublaminae. During t…

Retinagenetic structuresbiologyGeneral NeuroscienceRetinalInner plexiform layerAcetylcholinesteraseeye diseasesGanglionchemistry.chemical_compoundmedicine.anatomical_structurechemistryKnockout mousemedicinebiology.proteinsense organsCalretininNeuroscienceParvalbuminEuropean Journal of Neuroscience
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