Search results for "Cell adhesion"

showing 10 items of 812 documents

Effects of chronic fluoxetine treatment on the rat somatosensory cortex: Activation and induction of neuronal structural plasticity

2009

Recent hypotheses support the idea that disruption of normal neuronal plasticity mechanisms underlies depression and other psychiatric disorders, and that antidepressant treatment may counteract these changes. In a previous report we found that chronic fluoxetine treatment increases the expression of the polysialylated form of the neural cell adhesion molecule (PSA-NCAM), a molecule involved in neuronal structural plasticity, in the somatosensory cortex. In the present study we intended to find whether, in fact, cell activation and neuronal structural remodeling occur in parallel to changes in the expression of this molecule. Using immunohistochemistry, we found that chronic fluoxetine trea…

MaleNeuronsNeuronal PlasticityDose-Response Relationship DrugGeneral NeuroscienceCentral nervous systemHippocampusSomatosensory CortexBiologySomatosensory systemRatsRats Sprague-Dawleymedicine.anatomical_structurenervous systemFluoxetineApical dendriteNeuroplasticitymedicineAnimalsAntidepressive Agents Second-GenerationNeural cell adhesion moleculeCell activationPrefrontal cortexNeuroscienceNeuroscience Letters
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PSA-NCAM expression in the rat medial prefrontal cortex

2005

The rat medial prefrontal cortex, an area considered homologous to the human prefrontal cortex, is a region in which neuronal structural plasticity has been described during adulthood. Some plastic processes such as neurite outgrowth and synaptogenesis are known to be regulated by the polysialylated form of the neural cell adhesion molecule (PSA-NCAM). Since PSA-NCAM is present in regions of the adult CNS which are undergoing structural remodeling, such as the hypothalamus or the hippocampus, we have analyzed the expression of this molecule in the medial prefrontal cortex of adult rats using immunohistochemistry. PSA-NCAM immunoreactivity was found both in cell bodies and in the neuropil of…

MaleNeuropilNeuriteInterneuronAntimetabolitesCell SurvivalSynaptophysinSynaptogenesisPrefrontal CortexHippocampusNeural Cell Adhesion Molecule L1BiologyRats Sprague-DawleyNeuroplasticityNeuropilmedicineAnimalsFluorescent Antibody Technique IndirectPrefrontal cortexNeuronsNeuronal PlasticityGlutamate DecarboxylasePyramidal CellsGeneral NeuroscienceImmunohistochemistryRatsPhenotypemedicine.anatomical_structureBromodeoxyuridinenervous systemSialic AcidsNeural cell adhesion moleculeNeuroscienceNeuroscience
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The Role of Transforming Growth Factor-β1 in Airway Inflammation of Childhood Asthma

2013

TGF-beta-targeting structural and inflammatory cells has been implicated in the mechanisms leading to the inflammatory and restructuring processes in asthma, suggesting an impact of TGF-beta1 signaling on the development and persistency of this disease. We investigated the potential early involvement of TGF-beta1 activity in the immunological and molecular mechanisms underlying progression of inflammation in childhood asthma. We evaluated the levels of TGF-beta1 in induced sputum supernatants (ISSs) and the expression of small mother cell against decapentaplegic (Smad) 2 and Smad7 proteins in induced sputum cells (ISCs) from children with intermittent asthma (IA), moderate asthma (MA) and c…

MaleNeutrophilsSmad2 ProteinSMADEosinophilAdrenal Cortex HormoneSeverity of Illness IndexAdrenal Cortex HormonesImmunology and AllergyAge FactorPhosphorylationChildLungNeutrophilAge FactorsBronchodilator Agentsmedicine.anatomical_structureFemalemedicine.symptomCase-Control StudieHumanSignal TransductionGranulocyte activationAdolescentImmunologyAge Factors; Humans; Child; Macrophage-1 Antigen; Adrenal Cortex Hormones; Granulocytes; Neutrophils; Phosphorylation; Eosinophils; Adolescent; Signal Transduction; Male; Severity of Illness Index; Respiratory Mucosa; Asthma; Transforming Growth Factor beta1; Epithelial Cells; Lung; Smad2 Protein; Case-Control Studies; Smad7 Protein; Sputum; Administration Inhalation; Bronchodilator Agents; Cell Line; Female; Cell AdhesionMacrophage-1 AntigenCD18InflammationRespiratory MucosaGranulocyteCell LineSmad7 ProteinTransforming Growth Factor beta1Administration InhalationCell AdhesionmedicineHumansCell adhesionBronchodilator AgentPharmacologyEpithelial Cellbusiness.industrySputumGranulocyteEpithelial CellsEosinophilAsthmaEosinophilsCase-Control StudiesImmunologySputumbusinessGranulocytesInternational Journal of Immunopathology and Pharmacology
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Chronic fluoxetine treatment alters the structure, connectivity and plasticity of cortical interneurons

2014

Novel hypotheses suggest that antidepressants, such as the selective serotonin reuptake inhibitor fluoxetine, induce neuronal structural plasticity, resembling that of the juvenile brain, although the underlying mechanisms of this reopening of the critical periods still remain unclear. However, recent studies suggest that inhibitory networks play an important role in this structural plasticity induced by fluoxetine. For this reason we have analysed the effects of a chronic fluoxetine treatment in the hippocampus and medial prefrontal cortex (mPFC) of transgenic mice displaying eGFP labelled interneurons. We have found an increase in the expression of molecules related to critical period pla…

MalePERINEURONAL NET EXPRESSIONTime FactorsDendritic spinePSA-NCAMCritical period plasticityHippocampusCell CountADULT BRAIN PLASTICITYTREATMENT INCREASESHippocampusMice0302 clinical medicinePharmacology (medical)Prefrontal cortexCerebral Cortex0303 health sciencesNeuronal PlasticitybiologyGlutamate DecarboxylaseMEDIAL PREFRONTAL CORTEXPOLYSIALIC ACIDmusculoskeletal neural and ocular physiologyPerineuronal net3. Good healthPsychiatry and Mental healthParvalbuminsmedicine.anatomical_structureCerebral cortexCELL-ADHESION MOLECULEAntidepressive Agents Second-GenerationDendritic SpinesGreen Fluorescent ProteinseducationMice TransgenicNerve Tissue ProteinsNeural Cell Adhesion Molecule L1Inhibitory postsynaptic potentialRAT HIPPOCAMPUS03 medical and health sciencesmedicineAnimalsPSA-NCAM EXPRESSION030304 developmental biologyPharmacologyperineuronal netsinterneuronsCENTRAL-NERVOUS-SYSTEMfluoxetine3112 NeurosciencesGene Expression Regulationnervous systemVesicular Glutamate Transport Protein 1Sialic Acidsbiology.proteinNeural cell adhesion moleculeNerve NetNeuroscience030217 neurology & neurosurgeryParvalbuminThe International Journal of Neuropsychopharmacology
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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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Clinicopathological and immunohistochemical analysis of 20 cases of Merkel cell carcinoma in search of prognostic markers.

2005

Aims:  To evaluate the clinicopathological and immunohistochemical characteristics of Merkel cell carcinoma (MCC) in an attempt to find new, potentially significant, prognostic markers. Methods and results:  Clinical data and follow-up, histopathological features (pattern, cell size, thickness, mitoses, vascular invasion, lymphocytic infiltration) and immunohistochemical detection [CK20, thyroid transcription factor (TTF-1), chromogranin A, synaptophysin, p53, Ki67, Fli-1, CD99, c-Kit] were evaluated in 20 cases of MCC. Fli-1 and CD99 were detected in 90% and 55% of cases, respectively. Tumour size > 30 mm, stage II, ‘absent’ lymphocytic infiltration, and the presence of > 50% of Ki67+ tumo…

MalePathologyThyroid Nuclear Factor 1Keratin-20Intermediate Filament ProteinsLymph nodeAged 80 and overbiologyMerkel cell carcinomaChromogranin ANuclear ProteinsGeneral MedicineMiddle AgedPrognosisImmunohistochemistryDNA-Binding ProteinsProto-Oncogene Proteins c-kitmedicine.anatomical_structureFemaleMerkel cellmedicine.medical_specialtyHistologyCD99Synaptophysin12E7 AntigenPathology and Forensic MedicineAntigens CDProto-Oncogene ProteinsCarcinomamedicineBiomarkers TumorChromograninsHumansSurvival analysisAgedNeoplasm StagingProto-Oncogene Protein c-fli-1Keratin 20medicine.diseaseSurvival AnalysisCarcinoma Merkel CellMicroscopy ElectronKi-67 AntigenMultivariate Analysisbiology.proteinTrans-ActivatorsChromogranin ANeoplasm Recurrence LocalTumor Suppressor Protein p53Cell Adhesion MoleculesFollow-Up StudiesTranscription FactorsHistopathology
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Arterial and Venous Endothelia Display Differential Functional Fractalkine (CX 3 CL1) Expression by Angiotensin-II

2012

Objective— Angiotensin-II (Ang-II) promotes the interaction of mononuclear cells with arterioles and neutrophils with postcapillary venules. To investigate the mechanisms underlying this dissimilar response, the involvement of fractalkine (CX 3 CL1) was explored. Methods and Results— Enhanced CX 3 CL1 expression was detected in both cremasteric arterioles and postcapillary venules 24 hours after Ang-II intrascrotal injection. Arteriolar leukocyte adhesion was the unique parameter significantly reduced (83%) in animals lacking CX 3 CL1 receptor (CX 3 CR1). Human umbilical arterial and venous endothelial cell stimulation with 1 μmol/L Ang-II increased CX 3 CL1 expression, yet neutralization …

MalePathologyTime Factorsp38 Mitogen-Activated Protein KinasesMiceVenulesLeukocytesEndothelial dysfunctionExtracellular Signal-Regulated MAP KinasesReceptorCells CulturedMice KnockoutMembrane GlycoproteinsAngiotensin IINF-kappa BArteriesEndothelial stem cellArteriolesNADPH Oxidase 5NADPH Oxidase 4NADPH Oxidase 2FemaleRNA InterferenceReceptors ChemokineTumor necrosis factor alphaCardiology and Cardiovascular MedicineSignal Transductionmedicine.medical_specialtyCX3C Chemokine Receptor 1BiologyTransfectionPeripheral blood mononuclear cellLosartanVeinsInterferon-gammaApolipoproteins EDownregulation and upregulationInternal medicineCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansLeukocyte RollingCX3CL1Chemokine CX3CL1Tumor Necrosis Factor-alphaEndothelial CellsMembrane ProteinsNADPH OxidasesAtherosclerosismedicine.diseaseAngiotensin IIMice Inbred C57BLDisease Models AnimalEndocrinologyAngiotensin II Type 1 Receptor BlockersArteriosclerosis, Thrombosis, and Vascular Biology
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A Rare Cause of Persistent Rectal Bleeding.

2016

MalePathologymedicine.medical_specialtyBiopsyHemangiosarcomaMEDLINEColonoscopyAntigens CD3403 medical and health sciences0302 clinical medicineText miningBiopsymedicineBiomarkers TumorHumansVimentinAgedMicroscopyHepatologymedicine.diagnostic_testbusiness.industryHistocytochemistryRectal NeoplasmsGastroenterologyColonoscopyImmunohistochemistryPlatelet Endothelial Cell Adhesion Molecule-1Histocytochemistry030220 oncology & carcinogenesisImmunohistochemistry030211 gastroenterology & hepatologybusinessGastrointestinal HemorrhageClinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
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Analysis of human dysplastic haematopoiesis in long-term bone marrow culture

1989

In this paper we have analysed the behaviour of myelodysplastic marrow in a long-term bone marrow liquid culture system (LTBMC) from eleven patients with myelodysplastic syndromes with regard to cellularity, day-7 and day-14 CFU-GM growth, cluster formation, adherent cells and CFU-F formation. An altered CFU-GM pattern was found in 64% of cases at diagnosis, while normal growth was seen in the remaining cases, all of which were affected by refractory anaemia. The levels of CFU-GM, as well as cellularity, were reduced in myelodysplastic marrows compared to normal controls over the whole duration of LTBMCs. Cases with a normal CFU-GM level at diagnosis also showed pathological behaviour when …

MalePathologymedicine.medical_specialtyCFU-GMBiologyColony-Forming Units AssayInternal medicineCell AdhesionmedicineHumansPathologicalAgedErythroid Precursor CellsHematologyMyelodysplastic syndromesHematologyGeneral MedicineMiddle Agedmedicine.diseaseHematopoiesisKineticsHaematopoiesismedicine.anatomical_structureCell cultureMyelodysplastic SyndromesBone marrow cultureBone marrowBlut
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Immune escape mechanism: defective resting and stimulated leukocyte-endothelium interaction in hepatocellular carcinoma of the rat.

2004

Hepatocellular carcinoma represents an increasing therapeutic challenge due to its high incidence and early metastasis. Numerous studies have demonstrated the influence of the vascular system on tumor growth and development. In addition, the role of leukocyte-endothelium interaction in tumor vessels is of particular significance with regard to immunological tumor therapy. In this study we used an experimental in vivo animal model that allows a quantitative analysis on vessel morphology, microcirculation, and leukocyte-endothelium interaction. The vessel architecture in tumor tissue was found to be extremely heterogeneous, with a consecutively variable blood flow velocity. Following superfus…

MalePathologymedicine.medical_specialtyCell signalingCarcinoma HepatocellularEndotheliumPhysiologyCell CommunicationBiologyMetastasisMicrocirculationNeovascularizationmedicineLeukocytesAnimalsChemotactic FactorsNeovascularization PathologicCell adhesion moleculeMicrocirculationLiver NeoplasmsGastroenterologyHemodynamicsChemotaxismedicine.diseaseRatsRats Inbred ACImedicine.anatomical_structureLiverModels AnimalEndothelium Vascularmedicine.symptomLiver cancerCell Adhesion MoleculesBlood Flow VelocityDigestive diseases and sciences
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