Search results for "Disease Model"

showing 10 items of 1116 documents

EBI2 – Sensor for dihydroxycholesterol gradients in neuroinflammation

2018

Dihydroxycholesterols such as 7α,25-dihydroxysterols (7α,25-OHC) and 7α,27-OHC are generated from cholesterol by the enzymes CH25H, CYP7B1 and CYP27A1 in steady state but also in the context of inflammation. The G-protein coupled receptor (GPCR) Epstein-Barr virus-induced gene 2 (EBI2), also known as GPR183, senses these oxysterols and induces chemotactic migration of immune cells towards higher concentrations of these ligands. We recently showed that these ligands are upregulated in the CNS in experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis and that EBI2 enhanced early infiltration of encephalitogenic T cells into the CNS. In this short-review we dis…

0301 basic medicineEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisInflammationContext (language use)BiochemistryReceptors G-Protein-Coupled03 medical and health sciencesImmune systemmedicineAnimalsHumansReceptorNeuroinflammationInflammationImmunity CellularChemistryChemotaxisExperimental autoimmune encephalomyelitisGPR183ChemotaxisGeneral Medicinemedicine.diseaseHydroxycholesterolsCell biologyDisease Models Animal030104 developmental biologymedicine.symptomBiochimie
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T cells mediate autoantibody-induced cutaneous inflammation and blistering in epidermolysis bullosa acquisita

2016

AbstractT cells are key players in autoimmune diseases by supporting the production of autoantibodies. However, their contribution to the effector phase of antibody-mediated autoimmune dermatoses, i.e., tissue injury and inflammation of the skin, has not been investigated. In this paper, we demonstrate that T cells amplify the development of autoantibody-induced tissue injury in a prototypical, organ-specific autoimmune disease, namely epidermolysis bullosa acquisita (EBA) – characterized and caused by autoantibodies targeting type VII collagen. Specifically, we show that immune complex (IC)-induced inflammation depends on the presence of T cells – a process facilitated by T cell receptor (…

0301 basic medicineEpidermolysis bullosa acquisitamedicine.medical_specialtyCollagen Type VIINeutrophilsT-LymphocytesGene ExpressionMice NudeInflammationAntigen-Antibody ComplexCell CommunicationEpidermolysis Bullosa AcquisitaArticleMice03 medical and health sciencesCricetulus0302 clinical medicinemedicineAnimalsHumansAutoantibodiesSkinAutoimmune diseaseMice Inbred BALB CMultidisciplinarybusiness.industryT-cell receptorAutoantibodyAntibodies MonoclonalReceptors Antigen T-Cell gamma-deltamedicine.diseaseNatural killer T cellDermatologyImmune complexMice Inbred C57BLDisease Models Animal030104 developmental biologyLymphatic systemImmunoglobulin GImmunologyNatural Killer T-CellsLymph NodesRabbitsmedicine.symptombusinessSpleenSignal Transduction030215 immunologyScientific Reports
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Externalized decondensed neutrophil chromatin occludes pancreatic ducts and drives pancreatitis

2016

Ductal occlusion has been postulated to precipitate focal pancreatic inflammation, while the nature of the primary occluding agents has remained elusive. Neutrophils make use of histone citrullination by peptidyl arginine deiminase-4 (PADI4) in contact to particulate agents to extrude decondensed chromatin as neutrophil extracellular traps (NETs). In high cellular density, NETs form macroscopically visible aggregates. Here we show that such aggregates form inside pancreatic ducts in humans and mice occluding pancreatic ducts and thereby driving pancreatic inflammation. Experimental models indicate that PADI4 is critical for intraductal aggregate formation and that PADI4-deficiency abrogates…

0301 basic medicineExtracellular TrapsHydrolasesNeutrophilsScienceGeneral Physics and AstronomyBiologyExtracellular TrapsArticleGeneral Biochemistry Genetics and Molecular BiologyMice03 medical and health sciencesPancreatic JuiceProtein-Arginine Deiminase Type 4medicineAnimalsHumansPancreasCeruletideMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionQInterleukin-17Pancreatic DuctsGeneral ChemistryNeutrophil extracellular trapsFlow Cytometrymedicine.diseaseImmunohistochemistryChromatinCell biologyChromatinDisease Models AnimalHistone citrullination030104 developmental biologymedicine.anatomical_structurePancreatitisChronic DiseasePancreatic juiceImmunologyProtein-Arginine DeiminasesCytokinesPancreatitisPancreasCeruletideNature Communications
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Low-energy extracorporeal shockwave therapy (ESWT) improves metaphyseal fracture healing in an osteoporotic rat model.

2017

Purpose As result of the current demographic changes, osteoporosis and osteoporotic fractures are becoming an increasing social and economic burden. In this experimental study, extracorporeal shock wave therapy (ESWT), was evaluated as a treatment option for the improvement of osteoporotic fracture healing. Methods A well-established fracture model in the metaphyseal tibia in the osteoporotic rat was used. 132 animals were divided into 11 groups, with 12 animals each, consisting of one sham-operated group and 10 ovariectomized (osteoporotic) groups, of which 9 received ESWT treatment. Different energy flux intensities (0.15 mJ/mm2, 0.35 mJ/mm2, or 0.55 mJ/mm2) as well as different numbers o…

0301 basic medicineExtracorporeal Shockwave TherapyCritical Care and Emergency Medicinemedicine.medical_treatmentOsteoporosisTest StatisticsDentistryGene Expressionlcsh:MedicineRats Sprague-Dawley0302 clinical medicineMathematical and Statistical TechniquesAnimal CellsMedicine and Health SciencesReproductive System ProceduresConnective Tissue Diseaseslcsh:ScienceMusculoskeletal SystemTrauma MedicineConnective Tissue CellsFracture Healing030222 orthopedicsMultidisciplinaryBiomechanicsBone FractureConnective TissueExtracorporeal shockwave therapyPhysical SciencesOvariectomized ratFemaleAnatomyCellular TypesTraumatic InjuryStatistics (Mathematics)Research ArticleOvariectomySurgical and Invasive Medical ProceduresBone healingResearch and Analysis Methods03 medical and health sciencesRheumatologymedicineGeneticsAnimalsTibiaStatistical MethodsSkeletonAnalysis of VarianceOsteoblastsSurgical ExcisionTibiabusiness.industrylcsh:RBiology and Life SciencesBone fractureCell Biologymedicine.diseaseRatsDisease Models Animal030104 developmental biologyBiological TissueAdjunctive treatmentOsteoporosislcsh:QbusinessOsteoporotic FracturesMathematicsPLoS ONE
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Non-primate lentiviral vectors and their applications in gene therapy for ocular disorders

2018

Lentiviruses have a number of molecular features in common, starting with the ability to integrate their genetic material into the genome of non-dividing infected cells. A peculiar property of non-primate lentiviruses consists in their incapability to infect and induce diseases in humans, thus providing the main rationale for deriving biologically safe lentiviral vectors for gene therapy applications. In this review, we first give an overview of non-primate lentiviruses, highlighting their common and distinctive molecular characteristics together with key concepts in the molecular biology of lentiviruses. We next examine the bioengineering strategies leading to the conversion of lentiviruse…

0301 basic medicineEye DiseasesGenetic enhancementGenetic Vectorslcsh:QR1-502Settore BIO/11 - Biologia MolecolareReviewComputational biologyGenomelcsh:MicrobiologyLentiviruViral vectorEIAV03 medical and health sciences0302 clinical medicineGene therapyVirologyJDVAnimalsHumansZebrafishDrug CarrierZebrafishDrug CarriersBIVbiologyAnimalLentivirusCAEVEye DiseaseGenetic Therapybiology.organism_classificationFIVOphthalmologyDisease Models Animal030104 developmental biologyInfectious DiseasesVMVLentiviral vector030217 neurology & neurosurgeryHuman
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Shikonin Prevents Early Phase Inflammation Associated with Azoxymethane/Dextran Sulfate Sodium-Induced Colon Cancer and Induces Apoptosis in Human Co…

2018

Shikonin is the main active principle in the root of Lithospermum erythrorhizon, widely used in traditional Chinese medicine for its anti-inflammatory and wound healing properties. Recent research highlights shikonin's antitumor properties and capacity to prevent acute ulcerative colitis. The aim of the present study was to evaluate the ability of shikonin to prevent, in vivo, the early phases of colorectal cancer development, with special focus on its cytotoxic mechanism in vitro. We employed the azoxymethane/dextran sulfate sodium model of colitis in Balb/C mice. Body weight and drinking were monitored throughout the experiment, and length of colon and lesions of the colon were recorded o…

0301 basic medicineFarmacologíaAnti-Inflammatory AgentsAzoxymethanePharmaceutical ScienceCaspase 3ApoptosisPharmacologyPlant RootsAnalytical ChemistryProinflammatory cytokine03 medical and health scienceschemistry.chemical_compoundIn vivoDrug DiscoverymedicineAnimalsHumansColitisMedicine Chinese TraditionalPharmacologyInflammationMice Inbred BALB CWound HealingbiologyChemistryAzoxymethaneLithospermumOrganic ChemistryDextran Sulfatemedicine.diseaseInflammatory Bowel DiseasesNitric oxide synthaseDisease Models Animal030104 developmental biologyComplementary and alternative medicineCaco-2ApoptosisColonic Neoplasmsbiology.proteinMolecular MedicineColitis UlcerativeFemaleCaco-2 CellsNaphthoquinonesPlanta medica
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Higher physiopathogenicity byFasciola giganticathan by the genetically closeF. hepatica: experimental long-term follow-up of biochemical markers

2016

Background: Fascioliasis is caused by Fasciola hepatica and F. gigantica. The latter, always considered secondary in human infection, nowadays appears increasingly involved in Africa and Asia. Unfortunately, little is known about its pathogenicity, mainly due to difficulties in assessing the moment a patient first becomes infected and the differential diagnosis with F. hepatica. Methods: A long-term, 24-week, experimental study comparing F. hepatica and F. giganticawas made for the first time in the same animal model host, Guirra sheep. Serum biochemical parameters of liver damage, serum electrolytes, protein metabolism, plasma proteins, carbohydrate metabolism, hepatic lipid metabolism and…

0301 basic medicineFascioliasisMitochondrial DNAFasciola gigantica030231 tropical medicineAntibodies HelminthProtein metabolismSheep DiseasesPhysiologyCarbohydrate metabolismDiagnosis Differential03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSpecies SpecificityHepaticaparasitic diseasesAnimalsFasciola hepaticaBiochemical markersSheepbiologyPublic Health Environmental and Occupational HealthGeneral MedicineDNA Helminth030108 mycology & parasitologybiology.organism_classificationBlood proteinsFasciolaDisease Models AnimalInfectious DiseaseschemistryImmunoglobulin GParasitologyBiomarkersTransactions of The Royal Society of Tropical Medicine and Hygiene
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A specific prelimbic-nucleus accumbens pathway controls resilience versus vulnerability to food addiction

2019

Food addiction is linked to obesity and eating disorders and is characterized by a loss of behavioral control and compulsive food intake. Here, using a food addiction mouse model, we report that the lack of cannabinoid type-1 receptor in dorsal telencephalic glutamatergic neurons prevents the development of food addiction-like behavior, which is associated with enhanced synaptic excitatory transmission in the medial prefrontal cortex (mPFC) and in the nucleus accumbens (NAc). In contrast, chemogenetic inhibition of neuronal activity in the mPFC-NAc pathway induces compulsive food seeking. Transcriptomic analysis and genetic manipulation identified that increased dopamine D2 receptor express…

0301 basic medicineFood addictionSciencemedicine.medical_treatmentPrefrontal CortexAddictionGeneral Physics and AstronomyNucleus accumbensNeurotransmissionBiologySynaptic TransmissionNucleus AccumbensArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesGlutamatergic0302 clinical medicineReceptor Cannabinoid CB1Dopamine receptor D2Behavioural genetics ; AddictionNeural Pathwaysmental disordersmedicineAnimalsPremovement neuronal activitylcsh:SciencePrefrontal cortexMice KnockoutMultidisciplinaryReceptors Dopamine D2Gene Expression ProfilingQdigestive oral and skin physiologyFeeding BehaviorGeneral ChemistryUp-RegulationDisease Models Animal030104 developmental biologyGene Expression RegulationBehavioural geneticslcsh:QFood AddictionCannabinoidNeuroscience030217 neurology & neurosurgery
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ESC-Derived BDNF-Overexpressing Neural Progenitors Differentially Promote Recovery in Huntington's Disease Models by Enhanced Striatal Differentiation

2016

Summary Huntington's disease (HD) is characterized by fatal motoric failures induced by loss of striatal medium spiny neurons. Neuronal cell death has been linked to impaired expression and axonal transport of the neurotrophin BDNF (brain-derived neurotrophic factor). By transplanting embryonic stem cell-derived neural progenitors overexpressing BDNF, we combined cell replacement and BDNF supply as a potential HD therapy approach. Transplantation of purified neural progenitors was analyzed in a quinolinic acid (QA) chemical and two genetic HD mouse models (R6/2 and N171-82Q) on the basis of distinct behavioral parameters, including CatWalk gait analysis. Explicit rescue of motor function by…

0301 basic medicineGene ExpressionBiochemistrychemistry.chemical_compoundMice0302 clinical medicineNeural Stem CellsNeurotrophic factorsGenes Reporterlcsh:QH301-705.5Neuronslcsh:R5-920NeurogenesisCell DifferentiationAnatomyembryonic stem cellsHuntington Diseaselcsh:Medicine (General)NeurogliaLocomotionNeurotrophinHuntington’s diseaseCell SurvivalBiologyMedium spiny neuronArticle03 medical and health sciencesHuntington's diseaseGeneticsmedicinestriatal differentiationAnimalsBrain-derived neurotrophic factorBrain-Derived Neurotrophic FactorCell Biologymedicine.diseaseCorpus StriatumTransplantationDisease Models Animal030104 developmental biologylcsh:Biology (General)chemistrynervous systembiology.proteinNeuroscience030217 neurology & neurosurgeryBiomarkersDevelopmental BiologyQuinolinic acidStem Cell TransplantationStem Cell Reports
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Genetics and Gene Therapy of Anderson-Fabry Disease.

2018

Fabry's disease is a genetic disorder of X-linked inheritance caused by mutations in the alpha galactosidase A gene resulting in deficiency of this lysosomal enzyme. The progressive accumulation of glycosphingolipids, caused by the inadequate enzymatic activity, is responsible of organ dysfunction and thus of clinical manifestations. In the presence of a high clinical suspicion, a careful physical examination and specific laboratory tests are required, finally diagnosis of Fabry's disease is confirmed by the demonstration of absence or reduced alpha-galactosidase A enzyme activity in hemizygous men and gene typing in heterozygous females; in fact the performance of enzymatic activity assay …

0301 basic medicineGenetic enhancementChaperone therapyDisease030204 cardiovascular system & hematologyBioinformaticsMice0302 clinical medicineAlpha galactosidase ADrug DiscoveryGenetics (clinical)KidneybiologyTrihexosylceramidesGenetic disorderEnzyme replacement therapyDependovirusRecombinant ProteinsAlpha galactosidase A; Chaperone therapy; Enzyme replacement therapy; Fabry disease; Gene therapy; Viral vectors; Molecular Medicine; Molecular Biology; Genetics; Drug Discovery3003 Pharmaceutical Science; Genetics (clinical)Isoenzymesmedicine.anatomical_structureMolecular Medicinemedicine.symptomGenetic Vectors03 medical and health sciencesGene therapyViral vectorRare DiseasesGeneticGeneticsmedicineAnimalsHumansEnzyme Replacement TherapyMolecular BiologyAlpha-galactosidasebusiness.industryDrug Discovery3003 Pharmaceutical ScienceOrgan dysfunctionGenetic Therapymedicine.diseaseFabry diseaseDisease Models Animal030104 developmental biologyalpha-GalactosidaseMutationbiology.proteinFabry DiseasebusinessBiomarkersCurrent gene therapy
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