Search results for " Anima"

showing 10 items of 3536 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
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Sense and Antisense DMPK RNA Foci Accumulate in DM1 Tissues during Development.

2015

International audience; Myotonic dystrophy type 1 (DM1) is caused by an unstable expanded CTG repeat located within the DMPK gene 3'UTR. The nature, severity and age at onset of DM1 symptoms are very variable in patients. Different forms of the disease are described, among which the congenital form (CDM) is the most severe. Molecular mechanisms of DM1 are well characterized for the adult form and involve accumulation of mutant DMPK RNA forming foci in the nucleus. These RNA foci sequester proteins from the MBNL family and deregulate CELF proteins. These proteins are involved in many cellular mechanisms such as alternative splicing, transcriptional, translational and post-translational regul…

musculoskeletal diseasesCCAAT-Enhancer-Binding Protein-deltacongenital hereditary and neonatal diseases and abnormalities[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiologylcsh:MedicineMice Transgenic[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human genetics[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMyotonin-Protein KinaseMice[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]AnimalsHumansMyotonic DystrophyRNA AntisenseRNA Messengerlcsh:ScienceMuscle SkeletalCell NucleusMyocardiumlcsh:R[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyBrainGene Expression Regulation DevelopmentalRNA-Binding Proteins[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyEmbryo MammalianAlternative SplicingDisease Models Animal[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAnimals Newborn[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]lcsh:QTrinucleotide Repeat ExpansionSignal TransductionResearch ArticlePloS one
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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
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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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Patterns of trunk spine growth in two congeneric species of acanthocephalan: investment in attachment may differ between sexes and species.

2012

SUMMARYAcanthocephalans have evolved a hooked proboscis and some taxa have trunk spines to attach to their definitive hosts. These structures are generated before being used, thus a key question is how investment in attachment could optimally be allocated through the ontogeny. The number and arrangement of hooks and spines are never modified in the definitive host, but it is unclear whether these structures grow during adult development. A comparison of the size of trunk spines between cystacanths and adults of Corynosoma cetaceum and C. australe indicated that spines grow in both species, but only in females, which also had significantly larger spines than males. This sexual dimorphism did…

musculoskeletal diseasesMaleOntogenyDolphinsZoologyFlounderAcanthocephalaHost-Parasite InteractionsSpecies SpecificityAnimalsBody SizeSex CharacteristicsbiologyEcologyProboscismusculoskeletal systembiology.organism_classificationTrunkSpineSea LionsSexual dimorphismSpine (zoology)Infectious DiseasesPerchesKey (lock)Animal Science and ZoologyParasitologyFemaleAllometryHelminthiasis AnimalAcanthocephalaParasitology
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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
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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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