Search results for " mouse"

showing 10 items of 343 documents

Generation and functional analyses of hepatocyte-specific type I interleukin-1 receptor (IL-1RI) knockout mice

2016

medicine.anatomical_structureChemistryHepatocyteKnockout mouseGastroenterologymedicineInterleukin-1 receptorMolecular biologyZeitschrift für Gastroenterologie
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P087 Increased wnt ligands expression in M2c macrophages is associated with fibrosis in Stat6 knockout mice

2017

medicine.diagnostic_testbusiness.industryGastroenterologyWnt signaling pathwayGeneral Medicinemedicine.diseasePhenotypeFlow cytometryIntestinal mucosaFibrosisKnockout mousemedicineCancer researchSignal transductionbusinessSTAT6Journal of Crohn's and Colitis
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89. Loss of extinction in CA1-NMDA receptor deficient mice: A novel model for PTSD?

2009

medicine.medical_specialtyExtinctionEndocrinologyNeurologyChemistryPhysiology (medical)Internal medicinemedicineDeficient mouseNMDA receptorNeurology (clinical)Sensory SystemsClinical Neurophysiology
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Enhanced Age-Dependent ENOS Dysfunction and - Uncoupling in Glutathione Peroxidase-1-Deficient Mice

2012

medicine.medical_specialtyGPX1EndocrinologybiologyChemistryEnosPhysiology (medical)Internal medicineDeficient mousemedicineAge dependentbiology.organism_classificationBiochemistryFree Radical Biology and Medicine
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Genetic Deletion of JNK1 and JNK2 Aggravates the DSS-Induced Colitis in Mice

2007

The c-Jun N-terminal kinases (JNKs) are considered as novel targets for therapy of inflammatory bowel diseases (IBD). However, the relevant JNK isoforms have to be elucidated. Here, we analyze the individual contribution of the JNK1 and JNK2 isoforms in a dextran sulfate sodium (DSS) model of experimental colitis. JNK1 and JNK2 knockout mice (JNK1 ko, JNK2 ko) and their wild-type controls (WT1, WT2) received three cycles of DSS treatment, each consisting of 1.7% DSS for 5 days, followed by 5 days with water. Animals were daily evaluated by a disease activity index (DAI) comprising measurement of body weight, estimation of stool consistency, and test for occult blood/gross rectal bleeding. A…

medicine.medical_specialtyPathologyCryptApoptosisMice TransgenicInflammatory bowel diseaseGastroenterologyProinflammatory cytokineMiceCecumImmune systemInternal medicineWeight LossAnimalsMitogen-Activated Protein Kinase 9MedicineMitogen-Activated Protein Kinase 8Single-Blind MethodIntestinal MucosaColitisCrosses Geneticbusiness.industryDextran SulfateColitismedicine.diseaseMice Inbred C57BLmedicine.anatomical_structureApoptosisChronic DiseaseKnockout mouseSurgeryGastrointestinal HemorrhagebusinessJournal of Investigative Surgery
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Perivascular nerve fiber α-synuclein regulates contractility of mouse aorta: A link to autonomic dysfunction in Parkinson's disease

2010

Parkinson's disease and other neurodegenerative disorders associated to changes in alpha-synuclein often result in autonomic dysfunction, most of the time accompanied by abundant expression of this synaptic protein in peripheral autonomic neurons. Given that expression of alpha-synuclein in vascular elements has been previously reported, the present study was undertaken to determine whether alpha-synuclein directly participates in the regulation of vascular responsiveness. We detected by immunohistochemistry perivascular nerve fibers containing alpha-synuclein in the aorta of mice while aortic endothelial cells and muscular fibers themselves did not exhibit detectable levels of this protein…

medicine.medical_specialtyPresynaptic TerminalsAorta ThoracicVasodilationBiologyMuscle Smooth VascularMiceCellular and Molecular Neurosciencechemistry.chemical_compoundSympathetic Fibers PostganglionicDopaminemedicine.arteryInternal medicinemedicineAnimalsNeurotransmitterMice KnockoutAortaEndothelial CellsParkinson DiseaseCell Biologynervous system diseasesMice Inbred C57BLEndocrinologyAutonomic Nervous System Diseasesnervous systemchemistryVasoconstrictionKnockout mousealpha-SynucleinCatecholaminemedicine.symptomVasoconstrictionAcetylcholineMuscle Contractionmedicine.drugNeurochemistry International
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Repression of Cyclic Adenosine Monophosphate Upregulation Disarms and Expands Human Regulatory T Cells

2011

Abstract The main molecular mechanism of human regulatory T cell (Treg)-mediated suppression has not been elucidated. We show in this study that cAMP represents a key regulator of human Treg function. Repression of cAMP production by inhibition of adenylate cyclase activity or augmentation of cAMP degradation through ectopic expression of a cAMP-degrading phosphodiesterase greatly reduces the suppressive activity of human Treg in vitro and in a humanized mouse model in vivo. Notably, cAMP repression additionally abrogates the anergic state of human Treg, accompanied by nuclear translocation of NFATc1 and induction of its short isoform NFATc1/αA. Treg expanded under cAMP repression, however,…

medicine.medical_specialtyRegulatory T cellImmunologychemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryMicechemistry.chemical_compoundInternal medicineCyclic AMPmedicineAnimalsHumansImmunology and AllergyCyclic adenosine monophosphatePsychological repressionCell ProliferationClonal AnergyNFATC Transcription FactorsClonal anergyPhosphodiesterasehemic and immune systemsUp-RegulationCell biologyEndocrinologymedicine.anatomical_structurechemistryHumanized mousecAMP-dependent pathwayCyclase activityThe Journal of Immunology
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Effects of sodium fluoride on the mechanical activity in mouse gastric preparations.

2005

The aim of the present study was to investigate the responses induced by sodium fluoride (NaF) on gastric mechanical activity, using mouse whole-stomach preparations. The mechanical activity was recorded in vitro as changes of intraluminal pressure. In most of the preparations, NaF induced a tetrodotoxin-insensitive biphasic effect characterized by early relaxation followed by slowly developing contractile response. The contraction was dependent on the concentration of NaF, whereas the relaxation was observed at only 10–30 mmol/L NaF. The contractile effect was significantly reduced by nifedipine (an L-type Ca2+channel blocker), ryanodine or ruthenium red (inhibitors of Ca2+release from sar…

medicine.medical_specialtyRuthenium redPhysiologySettore BIO/09 - FisiologiaAdenylyl cyclasechemistry.chemical_compoundMiceNifedipinePhysiology (medical)Internal medicineSodium fluoridemedicineAnimalsChannel blockerEnzyme InhibitorsProtein Kinase CPharmacologyPhospholipase CRyanodine receptorStomachGastric mechanical activity Mouse stomach Smooth muscle Sodium fluorideMuscle SmoothGeneral MedicineNeomycinMice Inbred C57BLEndocrinologychemistryType C PhospholipasesAdenylyl Cyclase InhibitorsSodium FluorideCalciumExtracellular SpaceGastrointestinal Motilitymedicine.drugAdenylyl CyclasesMuscle ContractionCanadian journal of physiology and pharmacology
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p53 Involvement in the control of murine hair follicle regression.

2001

p53 is a transcription factor mediating a variety of biological responses including apoptotic cell death. p53 was recently shown to control apoptosis in the hair follicle induced by ionizing radiation and chemotherapy, but its role in the apoptosis-driven physiological hair follicle regression (catagen) remains to be elucidated. Here, we show that p53 protein is strongly expressed and co-localized with apoptotic markers in the regressing hair follicle compartments during catagen. In contrast to wild-type mice, p53 knockout mice show significant retardation of catagen accompanied by significant decrease in the number of apoptotic cells in the hair matrix. Furthermore, p53 null hair follicles…

medicine.medical_specialtyTumor suppressor genemedicine.medical_treatmentDown-RegulationApoptosisBiologyPathology and Forensic MedicineTelogen effluviumMiceBcl-2-associated X proteinDownregulation and upregulationInternal medicineProto-Oncogene ProteinsmedicineAnimalsbcl-2-Associated X ProteinMice Knockoutintegumentary systemGrowth factorAlopecia areatamedicine.diseaseHair follicleCell biologyUp-RegulationMice Inbred C57BLEndocrinologymedicine.anatomical_structureInsulin-Like Growth Factor Binding Protein 3Proto-Oncogene Proteins c-bcl-2Knockout mousebiology.proteinCommentaryFemaleTumor Suppressor Protein p53Hair FollicleThe American journal of pathology
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Abnormal development of pacinian corpuscles in double trkB;trkC knockout mice.

2006

Pacinian corpuscles depend on either Aalpha or Abeta nerve fibers of the large- and intermediate-sized sensory neurons for the development and maintenance of the structural integrity. These neurons express TrkB and TrkC, two members of the family of signal transducing neurotrophin receptors, and mice lacking TrkB and TrkC lost specific neurons and the sensory corpuscles connected to them. The impact of single or double targeted mutations in trkB and trkC genes in the development of Pacinian corpuscles was investigated in 25-day-old mice using immunohistochemistry and ultrastructural techniques. Single mutations on trkB or trkC genes were without effect on the structure and S100 protein expr…

medicine.medical_specialtyanimal structuresTropomyosin receptor kinase BBiologyTropomyosin receptor kinase CS100 proteinMiceMicroscopy Electron TransmissionInternal medicinemedicineLow-affinity nerve growth factor receptorAnimalsReceptor trkBReceptor trkCReceptorMice Knockoutmusculoskeletal neural and ocular physiologyGeneral NeuroscienceImmunohistochemistryCell biologyMice Inbred C57BLEndocrinologynervous systemAnimals NewbornTrk receptorembryonic structuresKnockout mousebiology.proteinPacinian CorpusclesNeurotrophinNeuroscience letters
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