Search results for "Intracellular"

showing 10 items of 821 documents

Endothelial Wnt/β-catenin signaling inhibits glioma angiogenesis and normalizes tumor blood vessels by inducing PDGF-B expression

2012

Wnt modulates glioma vascularization by regulating PDGF-B expression.

PathologyAngiogenesisCentral Nervous System NeoplasmsMice0302 clinical medicineImmunology and AllergyWnt Signaling Pathwaybeta Catenin0303 health sciencesbiologyNeovascularization PathologicBrain NeoplasmsWnt signaling pathwayIntracellular Signaling Peptides and ProteinsForkhead Transcription FactorsGliomaProto-Oncogene Proteins c-sis3. Good healthmedicine.anatomical_structureBlood-Brain Barrier030220 oncology & carcinogenesiscardiovascular systemIntercellular Signaling Peptides and ProteinsFemalemedicine.medical_specialtyBeta-cateninEndotheliumImmunologyNotch signaling pathwayMice NudeWnt1 ProteinMural cellArticle03 medical and health sciencesGliomamedicineAnimalsHumansddc:610neoplasms030304 developmental biologyAdaptor Proteins Signal TransducingCalcium-Binding ProteinsMembrane Proteinsmedicine.diseaseXenograft Model Antitumor Assaysnervous system diseasesDKK1Cancer researchbiology.proteinEndothelium VascularNeoplasm Grading
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IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease

2011

Interleukin (IL)-22 is an effector cytokine, which acts primarily on epithelial cells in the skin, gut, liver and lung. Both pro- and anti-inflammatory properties have been reported for IL-22 depending on the tissue and disease model. In a murine model of allergic airway inflammation, we found that IL-22 is predominantly produced by innate lymphoid cells in the inflamed lungs, rather than TH cells. To determine the impact of IL-22 on airway inflammation, we used allergen-sensitized IL-22-deficient mice and found that they suffer from significantly higher airway hyperreactivity upon airway challenge. IL-22-deficiency led to increased eosinophil infiltration lymphocyte invasion and production…

PathologyPulmonologymedicine.medical_treatmentT-LymphocytesIntracellular Spacelcsh:Medicine10263 Institute of Experimental ImmunologyInterleukin 22Mice0302 clinical medicineLymphocytesPhosphorylationlcsh:ScienceLung0303 health sciencesMultidisciplinaryInterleukin-13T CellsAllergy and HypersensitivityInnate lymphoid cellInterleukinrespiratory systemInnate ImmunityRecombinant Proteins3. Good healthCytokinemedicine.anatomical_structureInterleukin 13CytokinesMedicineTumor necrosis factor alphaBiological Markersmedicine.symptomResearch ArticleSTAT3 Transcription Factormedicine.medical_specialtyImmune CellsImmunologyAntigen-Presenting CellsImmunoglobulinsInflammation610 Medicine & health1100 General Agricultural and Biological SciencesBiology03 medical and health sciences1300 General Biochemistry Genetics and Molecular BiologymedicineRespiratory HypersensitivityAnimalsBiology030304 developmental biologyInflammation1000 MultidisciplinaryTumor Necrosis Factor-alphaInterleukinslcsh:RImmunityEpithelial CellsEosinophilAllergensAsthmaImmunity Innaterespiratory tract diseasesImmune SystemImmunology570 Life sciences; biologylcsh:QImmunizationBiomarkers030215 immunology
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Is antioxidant therapy effective to treat alzheimer's disease?

2011

Alzheimer’s disease (AD) is a neurodegenerative process associated with oxidative stress. In the past, it was claimed that all neuronal lesions involved in the onset and progression of AD were related to oxidative stress. Today, we know that intracellular amyloid beta (Ab) could play a central role in the pathophysiology of the disease. Ab binds to heme groups in mitochondrial membranes causing electron transport chain impairment and loss of respiratory function. The experimental evidence of such oxidative stress leads to the basis for treatment of AD with antioxidants. Many clinical trials have been developed to clarify whether antioxidants are beneficial in AD treatment. However, the resu…

Pathologymedicine.medical_specialtyAntioxidantbiologyAmyloid betamedicine.medical_treatmentDiseasemedicine.disease_causeBioinformaticsPathophysiologychemistry.chemical_compoundchemistrybiology.proteinmedicineRespiratory functionHemeIntracellularOxidative stressFree Radicals and Antioxidants
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Swelling, Acidosis, and Irreversible Damage of Glial Cells from Exposure to Arachidonic Acid in vitro

1994

Swelling and damage of C6 glioma cells and of primary cultured astrocytes were analyzed in vitro during incubation with arachidonic acid (AA; 20:4). The cells were suspended in a physiological medium supplemented with AA at concentrations of 0.001–1.0 m M. Cell swelling was quantified by flow cytometry with hydrodynamic focusing. Flow cytometry was also utilized for assessment of cell viability by exclusion of the fluorescent dye propidium iodide and for measurement of the intracellular pH (pHi) by 2′,7′-bis-(2-carboxyethyl)−5(and −6)carboxyfluorescein. Administration of AA caused an immediate dose-dependent swelling of C6 glioma cells, even at a concentration of 0.01 m M. At this level cel…

Pathologymedicine.medical_specialtyCell SurvivalLinoleic acidIntracellular pHBiologychemistry.chemical_compoundTumor Cells CulturedmedicineLactic AcidViability assayPropidium iodideCell damageArachidonic AcidFatty AcidsSodiumHydrogen-Ion Concentrationmedicine.diseaseMolecular biologyNeurologychemistryCell cultureAstrocytesLactatesSteroidsArachidonic acidNeurology (clinical)Swellingmedicine.symptomAcidosisCardiology and Cardiovascular MedicineNeurogliaJournal of Cerebral Blood Flow & Metabolism
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Endothelial nitric oxide synthase upregulation in the guinea pig organ of Corti after acute noise trauma.

2004

Endothelial nitric oxide synthase (eNOS) upregulation was identified 60 h after acute noise trauma in morphologically intact cells of the reticular lamina in the organ of Corti of the guinea pig in the second turn of the cochlea. Using gold-coupled anti-eNOS antibodies and electron microscopy, it was shown that eNOS expression was upregulated in all cell areas and cell types except inner hair cells. Furthermore, eNOS was found in the organelle-free cytoplasm and in mitochondria of various cell types. The density of eNOS in mitochondria was considerably higher compared with the surrounding cytoplasm. Since eNOS activity is regulated by calcium, the eNOS detection was combined with calcium pr…

Pathologymedicine.medical_specialtyCytoplasmNitric Oxide Synthase Type IIIGuinea Pigschemistry.chemical_elementCalciumMicrotubulesDownregulation and upregulationMicroscopy Electron TransmissionEnosStress PhysiologicalHair Cells AuditorymedicineAnimalsCalcium SignalingMolecular BiologyOrgan of CortiCytoskeletonbiologyGeneral NeuroscienceNitric Oxide Synthase Type IIIbiology.organism_classificationImmunohistochemistryCell biologyMitochondriaUp-RegulationNitric oxide synthaseActin CytoskeletonDisease Models Animalmedicine.anatomical_structureDrosophila melanogasterchemistryAcoustic StimulationHearing Loss Noise-InducedCytoplasmOrgan of Cortibiology.proteinCalciumNeurology (clinical)Nitric Oxide SynthaseNoiseIntracellularDevelopmental BiologyBrain research
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Young woman with Branchio-Oto-Renal Syndrome and a novel mutation in the EYA-1 gene

2011

Branchio-oto-renal (BOR) syndrome is an autosomal dominant disease clinically characterized by the coexistence of some or all of the following major disorders: deafness, cervical branchial fistulae, preauricular pits, and renal abnormalities. Most families with BOR syndrome have mutations on the EYA-1 gene on chromosome 8q. We present the case of a 23-year-old Italian woman without a familial history of BOR syndrome. The patient, who had hearing loss and a history of surgeries for correction of bilateral cervical branchial fistulae and bilateral preauricular pits, presented with renal impairment, hypertension and overt proteinuria. DNA sequencing showed a novel heterozygous mutation 1420-14…

Pathologymedicine.medical_specialtyHearing lossmedicine.disease_causeDiagnosis DifferentialYoung AdultExonChronic kidney diseaseCase reportmedicineHumansUltrasonographyBranchio-oto-renal syndromeMutationProteinuriabusiness.industryBranchio-oto-renal syndromeIntracellular Signaling Peptides and ProteinsNuclear ProteinsChromosomeAutosomal dominant traitGeneral MedicineEYA-1medicine.diseaseNephrologyMutationPreauricular pitFemaleProtein Tyrosine Phosphatasesmedicine.symptomTomography X-Ray Computedbusiness
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Functional spectrum of sinusoidal endothelial liver cells

1992

Pathologymedicine.medical_specialtyHepatologyEndotheliumPhagocytosisInflammationBiologyEndocytosisCell biologylaw.inventionEndothelial stem cellmedicine.anatomical_structureCell–cell interactionlawmedicinemedicine.symptomIntracellularFiltrationJournal of Hepatology
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Dextran sulfate sodium leads to chronic colitis and pathological angiogenesis in Endoglin heterozygous mice

2010

Pathological angiogenesis is an intrinsic component of chronic intestinal inflammation, which results in remodeling and expansion of the gut microvascular bed. Endoglin is essential for endothelial cell function and physiological angiogenesis. In this study we investigated its potential role in the regulation of inflammation by testing the response of Endoglin heterozygous (Eng(+/-)) mice to experimental colitis.C57BL/6 Eng(+/-) and littermate control mice drank water supplemented with 3% dextran sulfate sodium (DSS) for 5 days and were monitored for up to 26 days for clinical signs of colitis. Inflammation, crypt damage, and angiogenic index were scored on histological sections of distal c…

Pathologymedicine.medical_specialtyHeterozygoteAngiogenesisColonVascular permeabilityInflammatory bowel diseaseArticleNeovascularizationCapillary Permeabilitychemistry.chemical_compoundMicemedicineImmunology and AllergyAnimalsColitisAcute colitisNeovascularization Pathologicbusiness.industryVascular Endothelial Growth FactorsDextran SulfateGastroenterologyEndoglinIntracellular Signaling Peptides and ProteinsEndoglinmedicine.diseaseColitisVascular endothelial growth factorMice Inbred C57BLDisease Models AnimalchemistryAcute Diseasemedicine.symptombusinessAngiopoietins
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Cell viability, osteoblast differentiation, and gene expression are altered in human osteoblasts from hypertrophic fracture non-unions

2007

Recent studies have provided evidence that the number and proliferation capacity of bone marrow-derived mesenchymal stem cells, as well as the number of osteoprogenitor cells are reduced in patients with fracture non-unions. For fracture non-unions that do not heal after appropriate surgical intervention, the question arises as to what extent systemic cellular dysfunctions should be considered as being pathogenetic factors. For this purpose, we have examined the hypothesis that the cell function of osteoblasts isolated from patients with fracture non-unions may differ from those of normal control individuals in an identical and controlled in vitro situation. We analyzed the osteoblast cell …

Pathologymedicine.medical_specialtyHistologyCell SurvivalPhysiologyEndocrinology Diabetes and MetabolismCellular differentiationDown-RegulationBone healingBiologyModels BiologicalCalcification PhysiologicGene expressionmedicineHumansViability assayCells CulturedOligonucleotide Array Sequence AnalysisOsteoblastsReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingMesenchymal stem cellIntracellular Signaling Peptides and ProteinsWnt signaling pathwayCell DifferentiationOsteoblastAlkaline PhosphataseCell biologyGene expression profilingmedicine.anatomical_structureFractures UnunitedBone
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Anoxia in vitro does not induce neuronal swelling or death

1996

To improve the understanding of neuronal cell swelling in cerebral ischemia, cell volume regulation, viability, intracellular electrolytes, and lactate production of Neuro-2A neuroblastoma cells were studied using an in vitro model. The volume regulatory capacity of Neuro-2A cells was assessed after incubation in hypo- and hypertonic media. Anoxia was studied alone and together with inhibition of glycolysis by iodoacetate. Reducing the tonicity of the incubation medium to 250, 200, or 150 mosm/l caused immediate swelling followed by a regulatory volume decrease within 20 min, which, however, was not complete. The final cell volume after regulation depended on the tonicity of the medium and …

Pathologymedicine.medical_specialtyMetabolismBiologyNeurologyAnaerobic glycolysisExtracellular fluidBiophysicsmedicineTonicityGlycolysisNeurology (clinical)Viability assayAnaerobic exerciseIntracellularJournal of the Neurological Sciences
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