Search results for "NBR"

showing 10 items of 2710 documents

Comparison of the acute effects of anti-TNF-alpha drugs on a uveitis experimental model.

2010

To compare histopathological and biochemical effects of the anti-TNF-alpha drugs adalimumab and infliximab in a uveitis experimental model.Histopathological evaluation was performed 24 h after endotoxin (200 microg into the footpad) and drug administration, as well as biochemical analysis of oxidative stress-related markers in the aqueous humor.Severe inflammation was found in rat anterior chamber of the eye 24 h after endotoxin. Only infliximab administration partially prevented the endotoxin-induced disruption of the blood-aqueous barrier, as well as the increase in Rantes and MCP-1 concentration in aqueous humor. Both drugs ameliorated the histopathological score after endotoxin. Biochem…

musculoskeletal diseasesAcute effectsMaleBlood-Aqueous BarrierTime FactorsAnti-Inflammatory AgentsInflammationmedicine.disease_causeAntibodies Monoclonal HumanizedAqueous HumorUveitisAdalimumabImmunology and AllergyMedicineAnimalsskin and connective tissue diseasesCells Culturedbiologybusiness.industryTumor Necrosis Factor-alphaAdalimumabAntibodies Monoclonalmedicine.diseaseInfliximabInfliximabRatsOphthalmologyDisease Models AnimalOxidative StressTreatment OutcomeRats Inbred LewImmunologyMonoclonalbiology.proteinAntibodymedicine.symptombusinessOxidative stressUveitismedicine.drugOcular immunology and inflammation
researchProduct

Gastric emptying, small intestinal transit and fecal output in dystrophic (mdx) mice.

2009

Duchenne muscular dystrophy (DMD), which results from deficiency in dystrophin, a sarcolemma protein of skeletal, cardiac and smooth muscle, is characterized by progressive striated muscle degeneration, but various gastrointestinal clinical manifestations have been observed. The aim was to evaluate the possible impact of the dystrophin loss on the gastrointestinal propulsion in mdx mice (animal model for DMD). The gastric emptying of a carboxymethyl cellulose/phenol red dye non-nutrient meal was not significantly different at 20 min from gavaging between wild-type and mdx mice. The intestinal transit and the fecal output were significantly decreased in mdx versus normal animals, although th…

musculoskeletal diseasesCell physiologyDuchenne muscular dystrophyMalecongenital hereditary and neonatal diseases and abnormalitiesmdx mousemedicine.medical_specialtyPhysiologyDuchenne muscular dystrophySettore BIO/09 - FisiologiaMiceIn vivoInternal medicineIntestine SmallMedicineAnimalsmdx mouseMuscular dystrophyDefecationSarcolemmabiologyGastric emptyingbusiness.industryMuscular Dystrophy Animalmusculoskeletal systemmedicine.diseaseMice Inbred C57BLDisease Models AnimalEndocrinologyGastric Emptyingbiology.proteinFecal outputMice Inbred mdxIntestinal transitbusinessDystrophinGastrointestinal MotilityThe journal of physiological sciences : JPS
researchProduct

Targeting of the transcription factor STAT4 by antisense phosphorothioate oligonucleotides suppresses collagen-induced arthritis

2007

Abstract The transcription factor STAT4 mediates signals of various proinflammatory cytokines, such as IL-12, IL-15, and IL-23, that initiate and stabilize Th1 cytokine production. Although Th1 cytokine production has been suggested to play a major pathogenic role in rheumatoid arthritis, the role of STAT4 in this disease is poorly understood. In this study, we demonstrate a key functional role of STAT4 in murine collagen-induced arthritis (CIA). In initial studies we found that STAT4 expression is strongly induced in CD4+ T cells and to a lesser extent in CD11b+ APCs during CIA. To analyze the role of STAT4 for arthritis manifestation, we next investigated the outcome of interfering with S…

musculoskeletal diseasesImmunologyAntigen-Presenting CellsCodon InitiatorArthritisBiologyProinflammatory cytokineArthritis RheumatoidPathogenesisMiceimmune system diseasesmedicineAnimalsImmunology and Allergyskin and connective tissue diseasesSTAT4Cells CulturedMice KnockoutMice Inbred BALB CCD11b Antigenhemic and immune systemsOligonucleotides AntisenseSTAT4 Transcription FactorTh1 CellsThionucleotidesmedicine.diseaseArthritis ExperimentalIntegrin alpha MRheumatoid arthritisImmunologybiology.proteinExperimental pathologyTumor necrosis factor alpha
researchProduct

H2-M polymorphism in mice susceptible to collagen-induced arthritis involves the peptide binding groove.

1996

The ability to develop type II collagen (CII)-induced arthritis (CIA) in mice is associated with the major histocompatibilityI-A gene and with as yet poorly defined regulatory molecules of the major histocompatibility complex (MHC) class II antigen processing and presentation pathway. H2-M molecules are thought to be involved in the loading of antigenic peptides into the MHC class II binding cleft. We sequencedH2-Ma, H2-Mb1, andH2-Mb2 genes from CIA-susceptible and-resistant mouse strains and identified four differentMa andMb2 alleles and three differentMb1 alleles defined by polymorphic residues within the predicted peptide binding groove. Most CIA-resistant mouse strains share commonMa, M…

musculoskeletal diseasesImmunologyGenes MHC Class IIMolecular Sequence DataGenes MHC Class IPeptide bindingMice Inbred StrainsMajor histocompatibility complexEpitopeMiceAntigenMHC class IGeneticsAnimalsAmino Acid SequencePhylogenyDNA PrimersMHC class IIPolymorphism GeneticbiologyBase SequenceSequence Homology Amino AcidAntigen processingH-2 AntigensHistocompatibility Antigens Class IIMolecular biologyArthritis ExperimentalHistocompatibilityHaplotypesbiology.proteinCollagenSequence AlignmentImmunogenetics
researchProduct

Altered (oxidized) C1q induces a rheumatoid arthritis-like destructive and chronic inflammation in joint structures in arthritis-susceptible rats.

1997

Previous studies have identified an altered C1q molecule in synovial fluids from the joints of rheumatoid arthritis patients. We therefore immunized arthritis-susceptible Lewis 1A.AVN rats with either native C1q (C1q nat), altered (oxidized) C1q (C1q ox), or type II collagen (CII, induces arthritis in these animals), in order to induce arthritis. Unlike C1q nat, both CII and C1q ox were able to induce swelling and erythema of joints consistent with an arthritis-like inflammatory reaction. Histopathological evaluation of individual joint sections revealed synovitis, bursitis and tendovaginitis, massive joint destruction, and severe pannus formation. In a time-course study, no differences in …

musculoskeletal diseasesImmunologyType II collagenArthritischemical and pharmacologic phenomenaInflammationPathology and Forensic Medicinefluids and secretionsAntigenimmune system diseasesSynovitismedicineImmunology and AllergyAnimalsskin and connective tissue diseasesAutoimmune diseaseInflammationbiologybusiness.industryArthritisComplement C1qmedicine.diseaseRatsRats Inbred LewRheumatoid arthritisImmunologybiology.proteinFemaleJointsmedicine.symptomAntibodybusinessOxidation-ReductionClinical immunology and immunopathology
researchProduct

Modulation of type II collagen-induced arthritis in DBA/1 mice by intravenous application of a peptide from the C1q-A chain.

1992

In this report we are able to show that intravenous (i.v.) application (day 0) of a nonapeptide (residues 26-34) from the human C1q A-chain (designated peptide A-C1q) prior to intradermal (i.d.) administration of chicken type II collagen (CII) in arthritis-susceptible DBA/1 mice (H2q), leads to abrogation of polymorphonuclear neutrophil (PMN) invasion into the joints. This nonapeptide exhibits epitope characteristics and high homology to residues 137-147 of CB11 (a cyanogen bromide fragment of chicken CII, known to contain both arthritis inducing and suppressing determinants). Arthritis index was lowest in animals pretreated i.v. with CII (as internal control), though animals pretreated i.v…

musculoskeletal diseasesMaleInjections IntradermalImmunologyMolecular Sequence DataType II collagenArthritischemical and pharmacologic phenomenaPeptideEpitopechemistry.chemical_compoundMiceAntigenAdjuvants ImmunologicmedicineImmunology and AllergyAnimalsAmino Acid Sequenceskin and connective tissue diseasesPeptide sequencechemistry.chemical_classificationbiologyArthritisComplement C1qHematologymedicine.diseaseMolecular biologyPeptide FragmentschemistryMice Inbred DBAImmunologyAntibody FormationInjections Intravenousbiology.proteinCyanogen bromideCollagenAntibodyOligopeptidesImmunobiology
researchProduct

Mechanical activity of small and large intestine in normal and mdx mice: a comparative analysis.

1999

The aim of this study was to compare the motor pattern (recorded as changes in intraluminal pressure) of isolated duodenum and proximal colon between dystrophic mdx and normal mice. When duodenal recordings from control preparations were compared with mdx mice there was no significant difference in the spontaneous motor pattern, responses to electrical nerve stimulation or sensitivity to pharmacological agents. Colonic segments from mdx mice showed a more complex motor pattern, consisting of contractions with amplitude and frequency similar to those of controls and by additional contractions with lower amplitude and higher frequency. Moreover, 70% of the colonic preparations from mdx mice d…

musculoskeletal diseasesMalecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyNerve stimulationPhysiologyColonDuodenumDuchenne muscular dystrophyIn Vitro TechniquesInhibitory postsynaptic potentialNitric oxidechemistry.chemical_compoundMiceReference ValuesInternal medicineIntestine SmallmedicineAnimalsLarge intestineProximal colonIntestine LargeEndocrine and Autonomic SystemsChemistrySignificant differenceGastroenterologyAnatomyMuscular Dystrophy Animalmusculoskeletal systemmedicine.diseaseElectric StimulationBiomechanical PhenomenaMice Inbred C57BLmedicine.anatomical_structureEndocrinologyDuodenumMice Inbred mdxGastrointestinal MotilityNeurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
researchProduct

Duodenal contractile activity in dystrophic (mdx) mice: reduction of nitric oxide influence.

2003

The present study was undertaken to analyse duodenal contractility in adult dystrophic (mdx) mice. The spontaneous changes of the isometric tension and the responses of longitudinal duodenal muscle to nonadrenergic, noncholinergic (NANC) nerve stimulation and to exogenous drugs were compared between normal and mdx mice. Duodenal segments from mdx mice displayed spontaneous contractions with higher frequency than normals. N omega-nitro-L-arginine methyl ester (L-NAME) increased the frequency of contractions in normals without affecting that in mdx mice. In normals, NANC nerve stimulation elicited a transient relaxation abolished by L-NAME. In mdx mice a frank relaxation was not observed, the…

musculoskeletal diseasesMalemedicine.medical_specialtyNerve stimulationPhysiologyDuodenumInhibitory pathwayIsometric exerciseIn Vitro TechniquesInhibitory postsynaptic potentialNitric OxideSettore BIO/09 - FisiologiaNitric oxideContractilityDystrophinchemistry.chemical_compoundMiceSmooth muscleInternal medicinemedicineSpontaneous contractionAnimalsNeuroscience (all)biologyDose-Response Relationship DrugEndocrine and Autonomic SystemsIntestinal relaxationGastroenterologymusculoskeletal systemMice Inbred C57BLEndocrinologychemistrybiology.proteinMice Inbred mdxmdx miceSodium nitroprussideDystrophinGastrointestinal Motilitytissuesmedicine.drugMuscle ContractionNeurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
researchProduct

Combined effect of AAV-U7-induced dystrophin exon skipping and soluble activin Type IIB receptor in mdx mice.

2012

Adeno-associated virus (AAV)-U7-mediated skipping of dystrophin-exon-23 restores dystrophin expression and muscle function in the mdx mouse model of Duchenne muscular dystrophy. Soluble activin receptor IIB (sActRIIB-Fc) inhibits signaling of myostatin and homologous molecules and increases muscle mass and function of wild-type and mdx mice. We hypothesized that combined treatment with AAV-U7 and sActRIIB-Fc may synergistically improve mdx muscle function. Bioactivity of sActRIIB-Fc on skeletal muscle was first demonstrated in wild-type mice. In mdx mice we show that AAV-U7-mediated dystrophin restoration improved specific muscle force and resistance to eccentric contractions when applied a…

musculoskeletal diseasesmdx mousemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesDuchenne muscular dystrophyActivin Receptors Type IIGenetic VectorsMyostatinBiologyDystrophin03 medical and health sciencesMice0302 clinical medicineInternal medicineGeneticsmedicineMyocyteAnimalsMuscular dystrophyMuscle SkeletalMolecular Biology030304 developmental biology0303 health sciencesBody WeightSkeletal muscleExonsGenetic TherapyDependovirusMuscular Dystrophy Animalmedicine.diseasemusculoskeletal system3. Good healthMice Inbred C57BLEndocrinologymedicine.anatomical_structureImmunologybiology.proteinMice Inbred mdxMolecular MedicineITGA7Dystrophin030217 neurology & neurosurgeryMuscle ContractionHuman gene therapy
researchProduct

Treatment with a CO-releasing molecule (CORM-3) reduces joint inflammation and erosion in murine collagen-induced arthritis.

2008

Contains fulltext : 70589.pdf (Publisher’s version ) (Closed access) OBJECTIVE: CO-releasing molecules (CO-RMs) are a novel class of anti-inflammatory agents. We have examined the possible therapeutic effects of CORM-3 in collagen-induced arthritis (CIA). METHODS: Arthritis was induced in DBA-1/J mice by type II collagen. Animals were treated with CORM-3 (5 and 10 mg/kg/day, intraperitoneally) or the inactive compound iCORM-3 (10 mg/kg/day, intraperitoneally) unable to release CO, from days 22 to 31. Production of anti-type II collagen antibodies, cytokines and cartilage olimeric matrix protein (COMP) was evaluated by enzyme-linked immunosorbent assay, and prostaglandin E(2) (PGE(2)) by rad…

musculoskeletal diseasesmedicine.medical_treatmentImmunologyAnti-Inflammatory AgentsDrug Evaluation PreclinicalType II collagenArthritisInflammationPharmacologyAuto-immunity transplantation and immunotherapy [N4i 4]DinoprostoneGeneral Biochemistry Genetics and Molecular BiologyMiceRheumatologyOrganometallic CompoundsPerception and Action [DCN 1]medicineAnimalsImmunology and AllergyChronic inflammation and autoimmunity [UMCN 4.2]Dose-Response Relationship Drugbiologybusiness.industryRANK LigandInterleukinIntercellular Adhesion Molecule-1medicine.diseaseArthritis ExperimentalPathogenesis and modulation of inflammation [N4i 1]Cellular infiltrationCyclooxygenase 2Mice Inbred DBARANKLImmunologybiology.proteinCytokinesTumor necrosis factor alphaMicrobial pathogenesis and host defense [UMCN 4.1]Inflammation Mediatorsmedicine.symptombusinessInfection and autoimmunity [NCMLS 1]Heme Oxygenase-1Immunity infection and tissue repair [NCMLS 1]Prostaglandin E
researchProduct