Search results for "blotting"

showing 10 items of 899 documents

Detection of Hepatitis B Virus DNA in the Liver of Children with Chronic Hepatitis B by In Situ Hybridization and Its Relation to Other Viral Markers

1992

The aim of the study was to detect hepatitis B virus (HBV) DNA by in situ hybridization (ISH) with a 35S-labeled radioactive probe in frozen liver biopsy tissue sections of 63 hepatitis B virus surface antigen (HBsAg)-positive children. The results were compared to other markers of viral replication. HBV DNA was detected in 48 children. Of the 15 negative cases, four had hepatitis B envelope antigen (HBeAg), 10 anti-HBe, and one neither HBeAg nor anti-HBe. Free HBV DNA in serum and liver was positive in one patient. Forty of the positive children were HBeAg- and six anti-HBe-positive; two were negative for both. Of 45 36 had HBV DNA in serum. In 38 of 47 HBV DNA and in 31 of 42 HBcAg could …

Genetic MarkersMaleHepatitis B virusHBsAgAdolescentHepatitis B virus DNA polymerasemedicine.disease_causemedicineHumansChildHepatitis B virusbiologymedicine.diagnostic_testGastroenterologyInfantNucleic Acid Hybridizationvirus diseasesHepatitis BHepatitis Bbiology.organism_classificationmedicine.diseaseHepatitis B Core AntigensVirologydigestive system diseasesBlotting SouthernHBcAgLiverHepadnaviridaeHBeAgChild PreschoolLiver biopsyChronic DiseaseDNA ViralPediatrics Perinatology and Child HealthFemaleJournal of Pediatric Gastroenterology and Nutrition
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Autosomal dominant polycystic kidney disease—in vitro culture of cyst-lining epithelial cells

1992

The major form of autosomal dominant polycystic kidney disease (ADPKD) in humans is linked to the PKD1 gene on chromosome 16p. The identity of the gene and the underlying pathogenetic mechanisms are not yet defined. Cyst-lining epithelial cells derived from a polycystic kidney were successfully grown in culture and designated MZ-PKD-1 cells. By linkage analysis, the related pedigree of the nephrectomized patient could be linked to the PKD1 gene on chromosome 16p. Thus, these cells exhibit the genotype of a mutated PKD1 gene and represent an in vitro culture model for ADPKD involving chromosome 16p. The antigenic phenotype was characterized immunohistologically by epithelial differentiation …

Genetic MarkersPathologymedicine.medical_specialtyAutosomal dominant polycystic kidney diseaseHLA-C AntigensBiologyEpitheliumGenetic linkagemedicineHumansNorthern blotGeneCells CulturedHLA-A AntigensPKD1urogenital systemAntibodies MonoclonalGeneral MedicineMiddle AgedBlotting NorthernPolycystic Kidney Autosomal Dominantmedicine.diseaseImmunohistochemistryMolecular biologyPhenotypePedigreeBlotMicroscopy ElectronPhenotypeHLA-B AntigensCell cultureFemaleChromosomes Human Pair 16Virchows Archiv B Cell Pathology Including Molecular Pathology
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Baculoviral display of functional scFv and synthetic IgG-binding domains.

2000

Viral vectors displaying specific ligand binding moities such as scFv fragments or intact antibodies hold promise for the development of targeted gene therapy vectors. In this report we describe baculoviral vectors displaying either functional scFv fragments or the synthetic Z/ZZ IgG binding domain derived from protein A. Display on the baculovirus surface was achieved via fusion of the scFv fragment or Z/ZZ domain to the N-terminus of gp64, the major envelope protein of the Autographa californica nuclear polyhedrosis virus, AcNPV. As examples of scFv fragments we have used a murine scFv specific for the hapten 2-phenyloxazolone and a human scFv specific for carcinoembryonic antigen. In pri…

Genetic enhancementvirusesRecombinant Fusion ProteinsBlotting WesternBiophysicschemical and pharmacologic phenomenaEnzyme-Linked Immunosorbent AssayVectors in gene therapySpodopteraBiochemistryViral vector03 medical and health sciencesMice0302 clinical medicineAntibody SpecificityPeptide LibraryAnimalsHumansMolecular BiologyImmunoglobulin FragmentsCells Cultured030304 developmental biology0303 health sciencesbiologyOxazoloneNuclear Polyhedrosis VirusCell Biologyrespiratory systembiology.organism_classificationMolecular biology3. Good healthCarcinoembryonic AntigenAutographa californicaIgG binding030220 oncology & carcinogenesisImmunoglobulin Gbiology.proteinBinding Sites AntibodyAntibodyHaptenBaculoviridaeHaptensViral Fusion ProteinsBiochemical and biophysical research communications
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Cholesterol and Amyloid-β: Evidence for a Cross-Talk between Astrocytes and Neuronal Cells.

2011

Accumulating data supports the concept that alterations of cholesterol metabolism might influence the development of Alzheimer's disease (AD), a neurodegenerative disorder characterized by progressive accumulation of amyloid-β (Aβ) peptides in the brain. Changes in the neuronal production of Aβ have been described as a function of cholesterol levels, thus suggesting a causal link between cholesterol homeostasis dysregulation and AD pathogenesis. Under physiological conditions, cholesterol uptake in the brain is efficiently prevented by the blood-brain barrier, and mature neurons are thought to rely on glial cells for their cholesterol supply. In the present study, we tested the hypothesis t…

Genetically modified mouseBlotting WesternEnzyme-Linked Immunosorbent AssayMice TransgenicCell LinePathogenesisMicechemistry.chemical_compoundAlzheimer DiseasemedicineAnimalsHomeostasisHumansBrain ChemistryNeuronsAmyloid beta-PeptidesbiologyCholesterolGeneral NeuroscienceTransporterReceptor Cross-TalkGeneral Medicinemedicine.diseaseCoculture TechniquesPsychiatry and Mental healthClinical PsychologyCholesterolATP Binding Cassette Transporter 1chemistryAstrocytesABCA1biology.proteinATP-Binding Cassette Transporterslipids (amino acids peptides and proteins)Geriatrics and GerontologyAlzheimer's diseaseNeuroscienceHomeostasisATP Binding Cassette Transporter 1
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Impairment of TGF-β signaling in T cells increases susceptibility to experimental autoimmune hepatitis in mice

2002

In autoimmune hepatitis, strong TGF-beta1 expression is found in the inflamed liver. TGF-beta overexpression may be part of a regulatory immune response attempting to suppress autoreactive T cells. To test this hypothesis, we determined whether impairment of TGF-beta signaling in T cells leads to increased susceptibility to experimental autoimmune hepatitis (EAH). Transgenic mice of strain FVB/N were generated expressing a dominant-negative TGF-beta type II receptor in T cells under the control of the human CD2 promoter/locus control region. On induction of EAH, transgenic mice showed markedly increased portal and periportal leukocytic infiltrations with hepatocellular necroses compared wit…

Genetically modified mouseCellular immunityPhysiologyT-LymphocytesEnzyme-Linked Immunosorbent AssayMice TransgenicAutoimmune hepatitisBiologyMiceImmune systemTransforming Growth Factor betaPhysiology (medical)medicineAnimalsHomeostasisCells CulturedAutoimmune diseaseHepatitisB-LymphocytesHepatologyGastroenterologyT lymphocyteBlotting Northernmedicine.diseaseImmunohistochemistryHepatitis AutoimmunePhenotypeNeutrophil InfiltrationImmunologySignal transductionSignal TransductionAmerican Journal of Physiology-Gastrointestinal and Liver Physiology
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Glycosylation deficiency at either one of the two glycan attachment sites of cellular prion protein preserves susceptibility to bovine spongiform enc…

2004

The conversion into abnormally folded prion protein (PrP) plays a key role in prion diseases. PrP(C) carries two N-linked glycan chains at amino acid residues 180 and 196 (mouse). Previous in vitro data indicated that the conversion process may not require glycosylation of PrP. However, it is conceivable that these glycans function as intermolecular binding sites during the de novo infection of cells on susceptible organisms and/or play a role for the interaction of both PrP isoforms. Such receptor-like properties could contribute to the formation of specific prion strains. However, in earlier studies, mutations at the glycosylation sites of PrP led to intracellular trafficking abnormalitie…

Genetically modified mouseGlycanGlycosylationGlycosylationPrionsanimal diseasesBovine spongiform encephalopathyMutantBlotting WesternScrapieMice TransgenicCHO CellsCell SeparationBiologyBiochemistryCell LinePrion Diseaseschemistry.chemical_compoundMicePolysaccharidesCell Line TumorCricetinaemedicineAnimalsImmunoprecipitationProtein IsoformsBiotinylationDisulfidesTransgenesCloning MolecularMolecular BiologyBinding SitesWild typeBrainCell Biologymedicine.diseaseFlow CytometryVirologyMolecular biologyIn vitronervous system diseasesEncephalopathy Bovine SpongiformMice Inbred C57BLchemistryMutationbiology.proteinCattleScrapieThe Journal of biological chemistry
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Increased Expression of β6-Integrin in Skin Leads to Spontaneous Development of Chronic Wounds

2004

Integrin alphavbeta6 is an epithelial cell-specific receptor that is not normally expressed by resting epithelium but its expression is induced during wound healing. The function of alphavbeta6-integrin in wound repair is not clear. In the present study, we showed that beta6-integrin expression was strongly up-regulated in the epidermis in human chronic wounds but not in different forms of skin fibrosis. To test whether increased beta6-integrin expression plays a role in abnormal wound healing we developed four homozygous transgenic mouse lines that constitutively expressed human beta6-integrin in the epithelium. The mice developed normally and did not show any histological abnormalities in…

Genetically modified mousePathologymedicine.medical_specialtyIntegrin beta ChainsMice TransgenicBiologyPolymerase Chain ReactionPathology and Forensic MedicineCicatrixMice03 medical and health sciences0302 clinical medicineTransforming Growth Factor betaFibrosismedicineAnimalsHumansIn Situ HybridizationSkin030304 developmental biologyWound Healing0303 health sciencesintegumentary systemEpidermis (botany)Transforming growth factor betamedicine.diseaseFibrosisImmunohistochemistryEpithelium3. Good healthBlotting Southernmedicine.anatomical_structure030220 oncology & carcinogenesisChronic Diseasebiology.proteinImmunohistochemistryWound healingRegular ArticlesTransforming growth factorThe American Journal of Pathology
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TGF-β Suppresses Tumor Progression in Colon Cancer by Inhibition of IL-6 trans-Signaling

2004

Alterations of TGF-beta signaling have been described in colorectal cancer, although the molecular consequences are largely unknown. By using transgenic mice overexpressing TGF-beta or a dominant-negative TGF-betaRII, we demonstrate that TGF-beta signaling in tumor infiltrating T lymphocytes controls the growth of dysplastic epithelial cells in experimental colorectal cancer, as determined by histology and a novel system for high-resolution chromoendoscopy. At the molecular level, TGF-beta signaling in T cells regulated STAT-3 activation in tumor cells via IL-6. IL-6 signaling required tumor cell-derived soluble IL-6R rather than membrane bound IL-6R and suppression of such TGF-beta-depende…

Genetically modified mouseSTAT3 Transcription FactorColorectal cancerRecombinant Fusion ProteinsT-LymphocytesImmunologyBlotting WesternEnzyme-Linked Immunosorbent AssayMice TransgenicProtein Serine-Threonine KinasesMiceIn vivoTransforming Growth Factor betamedicineImmunology and AllergyAnimalsHumansEndoscopy Digestive SystemIntestinal MucosaInterleukin 6Autocrine signallingMice KnockoutbiologyInterleukin-6Reverse Transcriptase Polymerase Chain ReactionReceptor Transforming Growth Factor-beta Type IIHistologymedicine.diseaseImmunohistochemistryReceptors Interleukin-6DNA-Binding ProteinsDisease Models AnimalInfectious DiseasesTumor progressionImmunologyColonic NeoplasmsCancer researchbiology.proteinDisease ProgressionTrans-ActivatorsReceptors Transforming Growth Factor betaTransforming growth factorSignal TransductionImmunity
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Mutated cylindromatosis gene affects the functional state of dendritic cells

2010

Cylindromatosis gene (CYLD) is a ubiquitously expressed deubiquitinating enzyme, which interacts with members of the NF-κB signaling pathway and attenuates NF-κB and JNK signaling. Here, we report that DC derived from transgenic mice, which solely express a naturally occurring CYLD isoform (CYLD(ex7/8)), display a higher content of nuclear RelB and express elevated levels of NF-κB family members as well as of known NF-κB-target genes comprising costimulatory molecules and pro-inflammatory cytokines, as compared with WT DC. Accordingly, unstimulated CYLD(ex7/8) DC exhibited a significantly higher primary allogenic T-cell stimulatory capacity than WT DC and exerted no tolerogenic activity. Tr…

Genetically modified mouseTransgeneBlotting WesternImmunologyMice TransgenicBiologyDexamethasoneDeubiquitinating enzymeSmall hairpin RNAMiceImmune ToleranceAnimalsImmunology and AllergyGlucocorticoidsMice KnockoutReverse Transcriptase Polymerase Chain ReactionTumor Suppressor ProteinsRELBTranscription Factor RelBNF-kappa BPeripheral toleranceCell DifferentiationDendritic CellsFlow CytometrySpecific Pathogen-Free OrganismsCell biologyIsoenzymesTranscription Factor AP-1MutationKnockout mouseImmunologybiology.proteinRNAFemaleSignal transductionSignal TransductionEuropean Journal of Immunology
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Naturally occurring autoantibodies interfere with β-amyloid metabolism and improve cognition in a transgenic mouse model of Alzheimer's disease 24 h …

2013

There is evidence that naturally occurring antibodies directed against Aβ (nAbs-Aβ) have a role in Aβ-metabolism and Aβ-clearance. The presence of nAbs-Aβ leads to a reduction in amyloid fibrillation and thus a reduction in their toxicity. We investigated the effects of nAbs-Aβ in respect to oligomerization and used the Tg2576 transgenic mouse model in order to investigate the rapid effect with a single-dose (24 h) on oligomer breakdown and cytokine secretion along with immunohistochemical characterization of synaptic plasticity. nAbs-Aβ were able to reduce toxic oligomer concentration with an increase in Aβ-monomers. Cytokine secretion was significantly reduced. Synaptic plasticity was als…

Genetically modified mousemedicine.medical_specialtytoxic oligomersAmyloidBlotting WesternEnzyme-Linked Immunosorbent AssayMice TransgenicBiologyAnimals Genetically ModifiedCellular and Molecular NeuroscienceMiceCognitionAlzheimer DiseaseInternal medicinemedicineAnimalsBiological PsychiatryAutoantibodiesAmyloid beta-Peptidesβ-amyloidbehaviorAutoantibodyAlzheimer's diseasemedicine.diseasenatural occurring autoantibodiesCell biologyPsychiatry and Mental healthDisease Models AnimalEndocrinologyinflammationSynaptic plasticityToxicitybiology.proteinCytokinesCytokine secretionOriginal ArticleFemaleAlzheimer's diseaseAntibodyTranslational Psychiatry
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