Search results for "Disease models"

showing 10 items of 1104 documents

Bacteria-specific cytotoxic CD8+ T cells: a missing link in the pathogenesis of the HLA-B27-associated spondylarthropathies.

1994

The term seronegative spondylarthropathies is used for an entity of rheumatic syndromes of peripheral joints and the spine (ankylosing spondylitis, reactive arthritis, Reiter's syndrome, arthritis in psoriasis and in inflammatory bowel disease) which are strongly associated with the MHC class I molecule HLA-B27. However, the mechanisms whereby HLA-B27 confers disease susceptibility have so far remained unknown. There is strong evidence that gut inflammation and infection with gram-negative bacteria play a role in the induction of B27-associated disease. HLA-B27, like other MHC class I molecules, physiologically binds antigenic peptides in its binding groove and presents them to CD8+ T lymph…

musculoskeletal diseasesCytotoxicity ImmunologicAnkylosisEpitopeEpitopesAntigenEnterobacteriaceaeMHC class IMedicineCytotoxic T cellAnimalsHumansSpondylarthropathiesHLA-B27 AntigenHLA-B27Antigens Bacterialbiologybusiness.industryArthritisSynovial MembraneGeneral MedicineDisease Models AnimalImmunologybiology.proteinBacterial antigenbusinessCD8Protein BindingT-Lymphocytes CytotoxicAnnals of medicine
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Deficiency of Nrf2 accelerates the effector phase of arthritis and aggravates joint disease

2011

14 páginas, 8 figuras, 1 tabla.-- et al.

musculoskeletal diseasesGenetically modified mouseMedicinaNF-E2-Related Factor 2PhysiologyChemokine CXCL1Clinical BiochemistryNitric Oxide Synthase Type IIArthritisMice Transgenicmedicine.disease_causeenvironment and public healthBiochemistryNrf2MicemedicineAnimalsMolecular BiologyGeneral Environmental SciencebiologyInterleukin-6Effectorbusiness.industryArthritisInflammation and degenerationCell Biologyrespiratory systemmedicine.diseaseArthritis ExperimentalInfection and autoimmunity Auto-immunity transplantation and immunotherapy [NCMLS 1]Disease Models AnimalOxidative StressEicosanoidCyclooxygenase 2Rheumatoid arthritisTumor Necrosis FactorsImmunologyOsteocalcinbiology.proteinGeneral Earth and Planetary SciencesJointsTumor necrosis factor alphaImmune Regulation Auto-immunity transplantation and immunotherapy [NCMLS 2]businessOxidation-ReductionHeme Oxygenase-1Oxidative stress
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COX-2 expression in chondrosarcoma: A role for celecoxib treatment?

2010

Chondrosarcomas are resistant to conventional chemo- and radiotherapy. A subset of chondrosarcomas arises secondarily in the benign tumour syndromes enchondromatosis (EC) and multiple osteochondromas (MO), and prevention of tumour development would greatly improve prognosis. We therefore investigated the effect of selective COX-2 inhibition on chondrosarcoma growth. COX-2 expression was studied in central- and peripheral cartilaginous tumours. The effect of COX-2 inhibition was assessed in four high-grade chondrosarcoma cell lines using celecoxib and NS-398 treatment. COX-2 activity (prostaglandin E-2 (PGE(2)) ELISA) and cell viability were measured. The (prophylactic) effect of celecoxib o…

musculoskeletal diseasesMaleCancer ResearchPathologymedicine.medical_specialtyCell Survivalmedicine.medical_treatmentChondrosarcomaDrug Evaluation PreclinicalMice NudeAntineoplastic AgentsBone NeoplasmsMiceIn vivomedicineTumor Cells CulturedAnimalsHumansViability assaySulfonamidesCyclooxygenase 2 Inhibitorsbusiness.industryCartilagemedicine.diseaseXenograft Model Antitumor AssaysRadiation therapyDisease Models Animalmedicine.anatomical_structureOncologyBone tumours Chondrosarcoma COX-2 inhibition Therapy Xenograft familial adenomatous polyposis cell-line cyclooxygenase-2 inhibitor trial tumors establishment emphasis origin boneCell cultureCelecoxibCyclooxygenase 2CelecoxibPyrazolesChondrosarcomabusinessmedicine.drugProstaglandin E
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FGFR2mutation in 46,XY sex reversal with craniosynostosis

2015

Patients with 46,XY gonadal dysgenesis (GD) exhibit genital anomalies, which range from hypospadias to complete male-to-female sex reversal. However, a molecular diagnosis is made in only 30% of cases. Heterozygous mutations in the human FGFR2 gene cause various craniosynostosis syndromes including Crouzon and Pfeiffer, but testicular defects were not reported. Here, we describe a patient whose features we would suggest represent a new FGFR2-related syndrome, craniosynostosis with XY male-to-female sex reversal or CSR. The craniosynostosis patient was chromosomally XY, but presented as a phenotypic female due to complete GD. DNA sequencing identified the FGFR2c heterozygous missense mutatio…

musculoskeletal diseasesMalemedicine.medical_specialtyGonadAdolescentDNA Mutational AnalysisMutation MissenseGonadal dysgenesisBiologymedicine.disease_causeCraniosynostosisXY gonadal dysgenesisCraniosynostosesMiceInternal medicineGeneticsmedicineAnimalsHumansMissense mutationGene Knock-In TechniquesReceptor Fibroblast Growth Factor Type 2Molecular BiologyGenetics (clinical)Gonadal Dysgenesis 46XYGeneticsMutationArticlesSyndromeGeneral MedicineSex reversalmedicine.diseaseMice Mutant StrainsDisease Models AnimalEndocrinologymedicine.anatomical_structurePfeiffer syndromeFemaleHuman Molecular Genetics
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Muscleblind, BSF and TBPH are mislocalized in the muscle sarcomere of a Drosophila myotonic dystrophy model

2012

SummaryMyotonic dystrophy type 1 (DM1) is a genetic disease caused by the pathological expansion of a CTG trinucleotide repeat in the 3' UTR of the DMPK gene. In the DMPK transcripts, the CUG expansions sequester RNA-binding proteins into nuclear foci, including transcription factors and alternative splicing regulators such as MBNL1. MBNL1 sequestration has been associated with key features of DM1. However, the basis behind a number of molecular and histological alterations in DM1 remain unclear. To help identify new pathogenic components of the disease, we carried out a genetic screen using a Drosophila model of DM1 that expresses 480 interrupted CTG repeats, i(CTG)480, and a collection of…

musculoskeletal diseasesSarcomerescongenital hereditary and neonatal diseases and abnormalitiesNeuroscience (miscellaneous)lcsh:MedicineMedicine (miscellaneous)RNA-binding proteinGenes InsectBiologyMyotonic dystrophyGeneral Biochemistry Genetics and Molecular BiologyAnimals Genetically Modifiedchemistry.chemical_compoundImmunology and Microbiology (miscellaneous)RNA interferencelcsh:PathologymedicineMBNL1AnimalsDrosophila ProteinsHumansMyotonic DystrophyGeneticsMuscleslcsh:RAlternative splicingNuclear ProteinsRNA-Binding ProteinsEpistasis Geneticmedicine.diseaseDisease Models AnimalchemistryGene Knockdown TechniquesDrosophilaFemaleRNA InterferenceTrinucleotide repeat expansionTrinucleotide Repeat ExpansionDrosophila Proteinlcsh:RB1-214Genetic screenResearch ArticleDisease Models & Mechanisms
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Non-conventional forms of HLA-B27 are expressed in spondyloarthritis joints and gut tissue

2016

Objectives Human leukocyte antigen (HLA)-B27 (B27) is the strongest genetic factor associated with development of Ankylosing Spondylitis and other spondyloarthropathies (SpA), yet the role it plays in disease pathogenesis remains unclear. We investigated the expression of potentially pathogenic non-conventional heavy chain forms (NC) of B27 in synovial and intestinal tissues obtained from SpA patients. We also determined the presence of NC-B27 in joints, lymphoid and gastrointestinal tissue from B27 transgenic (TG1) rats with M.tuberculosis-induced SpA. Methods Expression of NC-B27 in human SpA joints and gut and in (21-3 × 283-2)F1 HLA-B27/Huβ2m rat tissue was determined by immunohistochem…

musculoskeletal diseasesalpha-DefensinsHLA-B27 transgenic rat modelGastrointestinal DiseasesCD8 AntigensImmunologyGene ExpressionArticleSpondyloarthropathieAnimalsHumansHLA class I free-heavy chainImmunology and AllergySpondylitis AnkylosingSpondyloarthropathiesskin and connective tissue diseasesHLA-B27 AntigenHLA-B27CD11 AntigensHistocompatibility Antigens Class ISynovial MembraneReceptors KIR3DL2Arthritis ExperimentalR1HLA class I free-heavy chainsRatsDisease Models AnimalSettore MED/16 - ReumatologiaHLA class I free-heavy chains; HLA-B27; HLA-B27 transgenic rat model; Spondyloarthropathies; Immunology and Allergy; ImmunologyBone RemodelingRats Transgenic
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Aberrant glycosylation of alpha-dystroglycan causes defective binding of laminin in the muscle of chicken muscular dystrophy.

2005

Dystroglycan is a central component of dystrophin-glycoprotein complex that links extracellular matrix and cytoskeleton in skeletal muscle. Although dystrophic chicken is well established as an animal model of human muscular dystrophy, the pathomechanism leading to muscular degeneration remains unknown. We show here that glycosylation and laminin-binding activity of alpha-dystroglycan (alpha-DG) are defective in dystrophic chicken. Extensive glycan structural analysis reveals that Galbeta1-3GalNAc and GalNAc residues are increased while Siaalpha2-3Gal structure is reduced in alpha-DG of dystrophic chicken. These results implicate aberrant glycosylation of alpha-DG in the pathogenesis of mus…

musculoskeletal diseasesanimal structuresGlycosylationGlycosylationBiophysicsBiochemistryChromatography AffinityExtracellular matrixchemistry.chemical_compoundStructural BiologyLamininGeneticsDystroglycanmedicineAnimalsDystroglycanMuscular dystrophyDystrophic chickenDystroglycansMuscle SkeletalMolecular BiologybiologySkeletal muscleCell BiologyMuscular Dystrophy AnimalMuscular dystrophymedicine.diseaseMolecular biologycarbohydrates (lipids)Disease Models Animalmedicine.anatomical_structurechemistrybiology.proteinPikachurinLamininPlant LectinsITGA7ChickensProtein BindingFEBS letters
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Evaluation of efficacy and biocompatibility of a new absorbable synthetic substitute as a dural onlay graft in a large animal model.

2016

Numerous dura substitutes are commercially available, but no absorbable synthetic dura repair product has been used for both onlay and suture applications.The safety and effectiveness of a new absorbable synthetic substitute composed of Poly-L-lactide microfibers as onlay dural graft were evaluated.Physical properties and performance of the microfibrous synthetic dural substitute implanted as an onlay or suturable grafts were compared with these commercial products, including CODMAN ETHISORB™ Dura Patch and DuraGen™ Dural Graft Matrix, in a canine duraplasty model. The cerebrospinal fluid (CSF) leakage, macroscopic and microscopic observation at 30 and 90 days after implantation were invest…

musculoskeletal diseasesmedicine.medical_specialtyTime FactorsBiocompatibilityPolyesters02 engineering and technologyDural graftIn Vitro Techniques03 medical and health sciences0302 clinical medicineDogsDural substitutemedicineAnimalsCsf leakageCerebrospinal Fluid Leakbusiness.industryGeneral Medicine021001 nanoscience & nanotechnologynervous system diseasesSurgeryMicroscopic observationDisease Models AnimalNeurologyInlaysNeurology (clinical)Dura Mater0210 nano-technologybusiness030217 neurology & neurosurgeryLarge animalNeurological research
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Activation of the p38MAPK cascade is associated with upregulation of TNF alpha receptors in the spinal motor neurons of mouse models of familial ALS.

2005

Phosphorylated p38 mitogen-activated protein kinase (p38MAPK), but not activated c-jun-N-terminal kinase (JNK), increases in the motor neurons of transgenic mice overexpressing ALS-linked SOD1 mutants at different stages of the disease. This effect is associated with a selective increase of phosphorylated MKK3-6, MKK4 and ASK1 and a concomitant upregulation of the TNFalpha receptors (TNFR1 and TNFR2), but not IL1beta and Fas receptors. Activation of both p38 MAPK and JNK occurs in the activated microglial cells of SOD1 mutant mice at the advanced stage of the disease; however, this effect is not accompanied by the concomitant activation of the upstream kinases ASK1 and MKK3,4,6, while both …

p38 mitogen-activated protein kinasesMAP Kinase Kinase 3Mice TransgenicMAP Kinase Kinase 6BiologyMAP Kinase Kinase Kinase 5p38 Mitogen-Activated Protein KinasesReceptors Tumor Necrosis FactorCellular and Molecular NeuroscienceMiceSuperoxide Dismutase-1Downregulation and upregulationAnimalsHumansASK1RNA Messengerfas ReceptorPhosphorylationReceptorProtein kinase AMolecular BiologyP38MAPK cascadeMotor NeuronsKinaseSuperoxide DismutaseTumor Necrosis Factor-alphaAmyotrophic Lateral SclerosisJNK Mitogen-Activated Protein KinasesReceptors Interleukin-1Cell BiologyCell biologyEnzyme ActivationMice Inbred C57BLDisease Models AnimalTumor Necrosis Factor Decoy ReceptorsSpinal CordReceptors Tumor Necrosis Factor Type IDisease ProgressionTumor necrosis factor alphaSignal TransductionMolecular and cellular neurosciences
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A novel microtubule de-stabilizing complementarity-determining region C36L1 peptide displays antitumor activity against melanoma in vitro and in vivo

2015

AbstractShort peptide sequences from complementarity-determining regions (CDRs) of different immunoglobulins may exert anti-infective, immunomodulatory and antitumor activities regardless of the specificity of the original monoclonal antibody (mAb). In this sense, they resemble early molecules of innate immunity. C36L1 was identified as a bioactive light-chain CDR1 peptide by screening 19 conserved CDR sequences targeting murine B16F10-Nex2 melanoma. The 17-amino acid peptide is readily taken up by melanoma cells and acts on microtubules causing depolymerization, stress of the endoplasmic reticulum and intrinsic apoptosis. At low concentrations, C36L1 inhibited migration, invasion and proli…

rho GTP-Binding ProteinsMelanoma ExperimentalAntineoplastic AgentsApoptosisPeptideComplementarity determining regionBiologyEndoplasmic ReticulumMicrotubulesArticleMicePhosphatidylinositol 3-KinasesCell MovementTubulinCell Line TumormedicineAnimalsNeoplasm MetastasisMelanomaPI3K/AKT/mTOR pathwayCell Proliferationchemistry.chemical_classificationMultidisciplinaryInnate immune systemCell growthMelanomaIntrinsic apoptosisPTEN Phosphohydrolasemedicine.diseaseComplementarity Determining RegionsMolecular biologyMitochondriaDisease Models AnimalchemistryCell cultureCancer researchProtein MultimerizationPeptidesProto-Oncogene Proteins c-aktSignal TransductionScientific Reports
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