Search results for "Molecules"

showing 10 items of 1147 documents

Aspartoacylase-lacZ knockin mice: an engineered model of Canavan disease.

2011

Canavan Disease (CD) is a recessive leukodystrophy caused by loss of function mutations in the gene encoding aspartoacylase (ASPA), an oligodendrocyte-enriched enzyme that hydrolyses N-acetylaspartate (NAA) to acetate and aspartate. The neurological phenotypes of different rodent models of CD vary considerably. Here we report on a novel targeted aspa mouse mutant expressing the bacterial β-Galactosidase (lacZ) gene under the control of the aspa regulatory elements. X-Gal staining in known ASPA expression domains confirms the integrity of the modified locus in heterozygous aspa lacZ-knockin (aspa(lacZ/+)) mice. In addition, abundant ASPA expression was detected in Schwann cells. Homozygous (…

MaleCentral Nervous SystemCerebellumPathologyAnatomy and PhysiologyCanavan DiseaseMouseMutantlcsh:MedicineNeural HomeostasisBiochemistryMiceNeurobiology of Disease and Regenerationlcsh:ScienceSex CharacteristicsMultidisciplinaryNeuromodulationNeurochemistryGenomicsAnimal ModelsFunctional Genomicsmedicine.anatomical_structureLac OperonNeurologyHomeostatic MechanismsMedicineFemaleNeurochemicalsGenetic EngineeringResearch ArticleNervous System PhysiologyBiotechnologymedicine.medical_specialtyTransgeneCentral nervous systemNeurophysiologyMice TransgenicNeuroimagingBiologyNeurological SystemAmidohydrolasesWhite matterModel OrganismsGeneticsmedicineAnimalsBiologyNeuropeptidesLeukodystrophylcsh:RComputational Biologymedicine.diseaseMolecular biologyCanavan diseaseAspartoacylaseDisease Models AnimalMetabolismnervous systemSmall MoleculesCellular NeuroscienceMetabolic DisordersMutationGenetics of DiseaseNervous System Componentslcsh:QGene FunctionMolecular NeuroscienceAnimal GeneticsNeurosciencePLoS ONE
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Control of Cell Migration and Inflammatory Mediators Production by CORM-2 in Osteoarthritic Synoviocytes

2011

Background Osteoarthritis (OA) is the most widespread degenerative joint disease. Inflamed synovial cells contribute to the release of inflammatory and catabolic mediators during OA leading to destruction of articular tissues. We have shown previously that CO-releasing molecules exert anti-inflammatory effects in animal models and OA chondrocytes. We have studied the ability of CORM-2 to modify the migration of human OA synoviocytes and the production of chemokines and other mediators sustaining inflammatory and catabolic processes in the OA joint. Methodology/Principal Findings OA synoviocytes were stimulated with interleukin(IL)-1β in the absence or presence of CORM-2. Migration assay was…

MaleChemokineAnatomy and PhysiologyInterleukin-1betalcsh:MedicineGene ExpressionMatrix metalloproteinaseBiochemistryCell MovementDrug Discoverylcsh:ScienceMusculoskeletal SystemCells CulturedChemokine CCL2MultidisciplinarybiologyReverse Transcriptase Polymerase Chain ReactionSynovial MembraneNF-kappa BInterleukinCell migrationmedicine.anatomical_structureMedicineFemaleMatrix Metalloproteinase 3Inflammation MediatorsMatrix Metalloproteinase 1Mitogen-Activated Protein KinasesResearch ArticleCell PhysiologyBlotting WesternRheumatologySynovitisOsteoarthritisOrganometallic CompoundsmedicineHumansInterleukin 8BiologyAgedCell ProliferationChemokine CCL20lcsh:RInterleukin-8medicine.diseaseTranscription Factor AP-1CCL20Oxidative StressSmall MoleculesImmunologyCancer researchbiology.proteinlcsh:QSynovial membraneHeme Oxygenase-1PLoS ONE
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PSA-NCAM expression in the piriform cortex of the adult rat. Modulation by NMDA receptor antagonist administration.

2002

Administration of NMDA receptor antagonists upregulates the expression of the polysialylated form of the neural cell adhesion molecule (PSA-NCAM) in the adult hippocampus. Since the piriform cortex is also populated by PSA-NCAM immunoreactive neurons during adulthood, we sought to characterize them in detail and to test whether NMDA receptor antagonists also modulate PSA-NCAM in this cortical region. PSA-NCAM immunoreactivity is located mainly in layer II, where many neurogliaform and some pyramidal-semilunar transitional neurons are labeled. Many large neurons in layer III and endopiriform nucleus also express PSA-NCAM. Interestingly, some small labeled cells resembling migratory neuroblas…

MaleDoublecortin ProteinSynaptogenesisHippocampusNeural Cell Adhesion Molecule L1Receptors N-Methyl-D-AspartateRats Sprague-DawleyNeuroblastCell MovementPiriform cortexmedicineAnimalsMolecular BiologyNeural Cell Adhesion MoleculesNeuronsbiologyGeneral NeuroscienceOlfactory PathwaysDoublecortinRatsmedicine.anatomical_structurenervous systembiology.proteinSialic AcidsNeural cell adhesion moleculeNeurology (clinical)NeuNNeuroscienceNucleusExcitatory Amino Acid AntagonistsInjections IntraperitonealDevelopmental BiologyBrain research
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L-NAME induces direct arteriolar leukocyte adhesion, which is mainly mediated by angiotensin-II.

2005

Acute inhibition (1 h) of nitric oxide synthase (NOS) with L-NAME causes leukocyte recruitment in the rat mesenteric postcapillary venules that is angiotensin-II (Ang-II) dependent. Since 4-h exposure to Ang-II provokes arteriolar leukocyte adhesion, this study was designed to investigate whether subacute (4-h) NOS inhibition also causes this effect.Rats were intraperitoneally injected with saline, L-NAME, or 1H-[1,2,4]-oxidazolol-[4,3-a]-quinoxalin-1-one (ODQ). Leukocyte accumulation in the mesenteric microcirculation was examined 4 h later via intravital microscopy. Some groups were pretreated with losartan, an AT(1) Ang-II receptor antagonist.At 4-h, L-NAME caused a significant increase …

MaleEndotheliumPhysiologyPharmacologyLosartanNitric oxideRats Sprague-Dawleychemistry.chemical_compoundVenulesPhysiology (medical)medicineCell AdhesionLeukocytesAnimalsLeukocyte RollingSplanchnic CirculationReceptorMolecular BiologyAngiotensin II receptor type 1Microscopy VideobiologyAngiotensin IIAngiotensin IIRatsNitric oxide synthaseArteriolesmedicine.anatomical_structureLosartanNG-Nitroarginine Methyl EsterchemistryImmunologycardiovascular systembiology.proteinNitric Oxide SynthaseCardiology and Cardiovascular MedicineCell Adhesion MoleculesIntravital microscopymedicine.drugMicrocirculation (New York, N.Y. : 1994)
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Molecular basis of endothelial dysfunction in sepsis.

2003

Sepsis is one of the major causes of mortality in critically ill patients and develops as a result of the host response to infection. A complex network of events is set into motion in the body by the infection and results in the pathogenesis of sepsis. This review article focuses on the molecular mechanisms and components involved in the pathogenesis of sepsis with a major emphasis on the endothelium. This includes sepsis-inducing bacterial components (e.g. endotoxins), cellular targets of these molecules and their responses, host reactions, intracellular and cytokine networks, individual susceptibility and new therapeutic targets in sepsis treatment.

MaleEndotheliumPhysiologymedicine.medical_treatmentReceptors Cell SurfaceBiologyNitric OxidePathogenesisSepsisPhysiology (medical)SepsismedicineHumansEndothelial dysfunctionHypoxiaMembrane GlycoproteinsToll-Like ReceptorsEndothelial Cellsmedicine.diseaseReview articleBacterial adhesinEndotoxinsmedicine.anatomical_structureCytokineImmunologyMutationCytokinesFemaleDisease SusceptibilityEndothelium VascularCardiology and Cardiovascular MedicineReactive Oxygen SpeciesCell Adhesion MoleculesIntracellularInterleukin-1Cardiovascular research
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A "double hit" murine model for schizophrenia shows alterations in the structure and neurochemistry of the medial prefrontal cortex and the hippocamp…

2013

Both alterations in neurodevelopment and aversive experiences during childhood and adolescence seem important risk factors for schizophrenia. Animal models reproducing these alterations mimic some of the symptoms, constituting a valid approach to study the etiopathology of this disorder. Among these models, the perinatal injection of N-methyl-d-aspartate receptor antagonists and the postweaning social isolation rearing are among the most widely used. Our aim is to combine them in a "double hit" model, which should produce a wider spectrum of alterations. Lister Hooded rats have been subjected to a single injection of MK-801 at postnatal day 7 and socially isolated from postweaning to adulth…

MaleInterneuronHippocampusPrefrontal CortexNerve Tissue ProteinsAdult neurogenesisCalbindinHippocampuslcsh:RC321-571InterneuronNeurochemicalPregnancymedicineAnimalsAnimal modelPrefrontal cortexlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryNeural Cell Adhesion MoleculesbiologyBody Weightmedicine.diseaseRatsInhibitory neurotransmissionDisease Models Animalmedicine.anatomical_structureNeurologynervous systemAnimals NewbornGene Expression RegulationSocial IsolationSchizophreniabiology.proteinSchizophreniaFemaleCalretininDizocilpine MaleatePsychologyNeuroscienceExcitatory Amino Acid AntagonistsProto-Oncogene Proteins c-fosParvalbuminNeurobiology of disease
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Non-granule PSA-NCAM immunoreactive neurons in the rat hippocampus

2002

The polysialylated form of the neural cell adhesion molecule (PSA-NCAM) continues to be expressed in the adult hippocampus, mainly in a subset of neurons located in the innermost portion of the granule cell layer. PSA-NCAM immunoreactive neurons have also been described outside this layer in humans, where they are severely reduced in schizophrenic brains. Given this important clinical implication, we were interested in finding whether similar neurons existed in the adult rat hippocampus and to characterize their distribution, morphology and phenotype. PSA-NCAM immunocytochemistry reveals labeled neurons in the subiculum, fimbria, alveus, hilus, and stratum oriens, lucidum and radiatum of CA…

MaleInterneuronNeural Cell Adhesion Molecule L1Hippocampal formationHippocampusCalbindinImage Processing Computer-AssistedmedicineAnimalsNeuropeptide YFluorescent Antibody Technique IndirectNeural Cell Adhesion MoleculesMolecular Biologygamma-Aminobutyric AcidNeuronsbiologyGeneral NeuroscienceSubiculumGranule cellImmunohistochemistryRatsPhenotypemedicine.anatomical_structurenervous systemSialic Acidsbiology.proteinNeural cell adhesion moleculeNeurology (clinical)CalretininSomatostatinNeuroscienceParvalbuminDevelopmental BiologyBrain Research
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Carotenoid trade-off between parasitic resistance and sexual display: an experimental study in the blackbird (Turdus merula).

2008

Many parasites depress the expression of the carotenoid-based colour displays of their hosts, and it has been hypothesized that animals face a trade-off in carotenoid allocation between immune functions and ‘degree of ornamentation’. While numerous correlative studies suggest that parasite infection decreases the intensity of carotenoid-based colour displays, the existence of this trade-off has never been demonstrated experimentally in a host–parasite model. In this study, we used the blackbird ( Turdus merula ) and Isospora (an intestinal parasite) to assess whether this trade-off does indeed exist. Blackbirds were supplemented with carotenoids while simultaneously being exposed to parasi…

MaleMESH : Host-Parasite InteractionsMESH : Analysis of VarianceTrade-offmedicine.disease_causeSongbirds[ SDV.BBM.BC ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM][ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/SymbiosisParasite hostingbill colourCarotenoidGeneral Environmental Sciencetrade-offchemistry.chemical_classificationPigmentationMESH : PigmentationBeakcarotenoidsfood and beveragesMESH : IsosporaGeneral MedicineIsosporaBeakGeneral Agricultural and Biological SciencesResearch Article[ SDV.MP.PAR ] Life Sciences [q-bio]/Microbiology and Parasitology/ParasitologyMESH : MaleZoologyIntestinal parasiteBiologyParasitic infectionGeneral Biochemistry Genetics and Molecular BiologyHost-Parasite InteractionsCoccidiaBotanymedicineAnimalsBody Weights and MeasuresMESH : Dietary SupplementsMESH : SongbirdsMESH : CarotenoidsAnalysis of VarianceIsosporaGeneral Immunology and Microbiologyorganic chemicalscoccidiaMESH : Body Weights and Measuresbiology.organism_classificationMESH : Beakchemistryexperimental infectionDietary SupplementsMESH : Animals
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The Genome of the Sea Urchin Strongylocentrotus purpuratus

2006

We report the sequence and analysis of the 814-megabase genome of the sea urchin Strongylocentrotus purpuratus , a model for developmental and systems biology. The sequencing strategy combined whole-genome shotgun and bacterial artificial chromosome (BAC) sequences. This use of BAC clones, aided by a pooling strategy, overcame difficulties associated with high heterozygosity of the genome. The genome encodes about 23,300 genes, including many previously thought to be vertebrate innovations or known only outside the deuterostomes. This echinoderm genome provides an evolutionary outgroup for the chordates and yields insights into the evolution of deuterostomes.

MaleMESH: Signal TransductionMESH: Sequence Analysis DNAMESH : Transcription FactorsMESH : Calcification PhysiologicGenomeMESH : Proteins0302 clinical medicineMESH : Embryonic DevelopmentMESH: Gene Expression Regulation DevelopmentalInnateMESH: Embryonic DevelopmentDevelopmentalNervous System Physiological PhenomenaMESH: AnimalsMESH: Proteins[SDV.BDD]Life Sciences [q-bio]/Development BiologyComplement ActivationComputingMilieux_MISCELLANEOUSMESH: Evolution MolecularMESH : Strongylocentrotus purpuratusGenetics0303 health sciencesMESH: Nervous System Physiological PhenomenaMultidisciplinaryGenomebiologyMedicine (all)MESH: Immunologic FactorsGene Expression Regulation DevelopmentalGenome projectMESH: Transcription FactorsMESH : Immunity InnateMESH : Complement ActivationMESH: GenesBacterial artificial chromosome (BAC)DeuterostomesStrongylocentrotus purpuratusVertebrate innovationsEchinodermMESH : Nervous System Physiological Phenomenaembryonic structuresMESH: Cell Adhesion MoleculesMESH : GenesMESH: Immunity InnateSequence AnalysisSignal TransductionMESH: Computational BiologyGenome evolutionMESH: Complement ActivationSequence analysisEvolutionMESH: Strongylocentrotus purpuratusMESH : MaleEmbryonic DevelopmentMESH : Immunologic FactorsArticleMESH: Calcification PhysiologicCalcificationMESH : Cell Adhesion MoleculesEvolution Molecular03 medical and health sciencesCalcification PhysiologicAnimalsImmunologic FactorsMESH: Genome[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : Evolution MolecularPhysiologicGeneStrongylocentrotus purpuratus[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyMESH : Signal TransductionBacterial artificial chromosomeImmunityMolecularComputational BiologyProteinsAnimals; Calcification Physiologic; Cell Adhesion Molecules; Complement Activation; Computational Biology; Embryonic Development; Evolution Molecular; Gene Expression Regulation Developmental; Genes; Immunity Innate; Immunologic Factors; Male; Nervous System Physiological Phenomena; Proteins; Signal Transduction; Strongylocentrotus purpuratus; Transcription Factors; Genome; Sequence Analysis DNA; Medicine (all); MultidisciplinaryDNASequence Analysis DNAbiology.organism_classificationStrongylocentrotus purpuratusImmunity InnateMESH: MaleGene Expression RegulationGenesMESH : AnimalsMESH : Gene Expression Regulation DevelopmentalMESH : GenomeCell Adhesion Molecules030217 neurology & neurosurgeryMESH : Computational BiologyTranscription FactorsMESH : Sequence Analysis DNA
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Rare variants in the genetic background modulate cognitive and developmental phenotypes in individuals carrying disease-associated variants

2019

Purpose: To assess the contribution of rare variants in the genetic background toward variability of neurodevelopmental phenotypes in individuals with rare copy-number variants (CNVs) and gene-disruptive variants. Methods: We analyzed quantitative clinical information, exome sequencing, and microarray data from 757 probands and 233 parents and siblings who carry disease-associated variants. Results: The number of rare likely deleterious variants in functionally intolerant genes (“other hits”) correlated with expression of neurodevelopmental phenotypes in probands with 16p12.1 deletion (n=23, p=0.004) and in autism probands carrying gene-disruptive variants (n=184, p=0.03) compared with thei…

MaleParents0301 basic medicineProbandNeuronalGenetic Carrier Screening16p11.2 deletion030105 genetics & heredityCognitionFamily historyNeural Cell Adhesion MoleculesGenetics (clinical)Exome sequencingSequence DeletionGeneticsGenetic Carrier ScreeningPhenotypePenetrancePedigreePhenotypeAutistic Disorder/genetics; Autistic Disorder/physiopathology; Cell Adhesion Molecules Neuronal/genetics; Chromosomes Human Pair 16/genetics; Cognition/physiology; DNA Copy Number Variations/genetics; Female; Gene Expression Regulation/genetics; Genetic Background; Genetic Carrier Screening; Humans; Male; Methyltransferases/genetics; Nerve Tissue Proteins/genetics; Parents; Pedigree; Phenotype; Proteins/genetics; Sequence Deletion/genetics; Siblings; 16p11.2 deletion; CNV; autism; modifier; phenotypic variabilityFemaleGenetic BackgroundHumanDNA Copy Number VariationsCell Adhesion Molecules NeuronalCNVautismNerve Tissue ProteinsBiologyChromosomesArticle03 medical and health sciencesmental disordersmedicineHumansAutistic DisorderBiologyGenemodifierPair 16SiblingsCalcium-Binding ProteinsProteinsMethyltransferasesmedicine.disease16p11.2 deletion; autism; CNV; modifier; phenotypic variability; Genetics (clinical)Cytoskeletal Proteins030104 developmental biologyGene Expression Regulation[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutismphenotypic variabilityHuman medicine16p11.2 deletion; autism; CNV; modifier; phenotypic variability; Autistic Disorder; Cell Adhesion Molecules Neuronal; Chromosomes Human Pair 16; Cognition; DNA Copy Number Variations; Female; Gene Expression Regulation; Genetic Background; Humans; Male; Methyltransferases; Nerve Tissue Proteins; Parents; Pedigree; Phenotype; Proteins; Sequence Deletion; Siblings; Genetic Carrier ScreeningCell Adhesion MoleculesChromosomes Human Pair 16Transcription FactorsGenetics in Medicine
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