Search results for "Type I"

showing 10 items of 966 documents

New alkaloid antibiotics that target the DNA topoisomerase I of Streptococcus pneumoniae

2011

16 pags, 3 figs, 3 tabs

Models MolecularTopoisomerase-I Inhibitormedicine.disease_causeMicrobiologyBiochemistryCell LineMicrobiology03 medical and health scienceschemistry.chemical_compoundAlkaloidsBacterial ProteinsStreptococcus pneumoniaemedicineHumansAporphineMolecular BiologyEscherichia coli030304 developmental biologychemistry.chemical_classification0303 health sciencesDose-Response Relationship Drugbiology030306 microbiologyTopoisomeraseCell BiologyPhenanthrenesProtein Structure TertiaryAnti-Bacterial Agents3. Good healthStreptococcus pneumoniaeEnzymeDNA Topoisomerases Type IchemistryBiochemistrybiology.proteinDNA supercoilTopoisomerase I InhibitorsGrowth inhibitionJournal of Biological Chemistry 286: 6402-6413 (2011)
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Osteogenesis imperfecta type III : oral, craniofacial characteristics and atypical radiographic findings oral

2021

Osteogenesis imperfecta (OI) is a disease characterized by decreased bone mineral density, causing susceptibility to bone fractures by mild trauma and bone deformities. The aim of this study was to describe an osteogenesis imperfecta type III clinical case, its craniofacial and oral changes as well as its atypical radiographic findings. An eighteen-year-old, male patient diagnosed with osteogenesis imperfecta type III was referred for dental evaluation; the clinical examination showed the craniofacial and oral changes of the disease such as triangular face, class III malocclusion, anterior open bite and posterior crossbite, dentinogenesis imperfecta presenting amber discoloration. The radio…

Molarmedicine.diagnostic_testbusiness.industryDentinogenesis imperfectaRadiographyTriangular faceDentistryPhysical examinationCase Reportmedicine.diseaseOsteogenesis Imperfecta Type IIIstomatognathic diseasesstomatognathic systemOsteogenesis imperfectaMedicineOdontostomatology for the Disabled or Special PatientsCraniofacialbusinessGeneral DentistryUNESCO:CIENCIAS MÉDICAS
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A mild juvenile variant of type IV glycogenosis.

1992

The mild juvenile form of type IV glycogenosis, confirmed by a profound deficiency of the brancher enzyme in tissue specimens is reported from three Turkish male siblings who, foremost, suffered from chronic progressive myopathy. Muscle fibers contained polyglucosan inclusions of typical fine structure, i.e. a mixture of granular and filamentous glycogen. They reacted strongly for myophosphorylase, but were resistant to diastase. These inclusions were ubiquitinated and reacted with antibody KM-279 which previously has been shown to bind to Lafora bodies, corpora amylacea and polyglucosan material in hepatic and cardiac cells of type IV glycogenosis as well as polyglucosan body myopathy with…

Muscle tissueMalemedicine.medical_specialtyBiologychemistry.chemical_compoundGlycogen Storage Disease Type IVDevelopmental NeuroscienceInternal medicineSweat glandmedicineHumansGlycogen storage disease type IVMyopathyChildGlycogenStaining and LabelingHistocytochemistryMusclesInfantGeneral Medicinemedicine.diseaseEnzyme assaySweat Glandsmedicine.anatomical_structureEndocrinologychemistryMyophosphorylasePediatrics Perinatology and Child Healthbiology.proteinNeurology (clinical)medicine.symptomCorpora amylaceaBraindevelopment
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CXCR3-ligand-mediated skin inflammation in cutaneous lichenoid graft-versus-host disease.

2007

Background Lichenoid graft-versus-host disease (liGVHD) histologically shares several common features with other lichenoid dermatoses, such as cutaneous lupus erythematosus and lichen planus (LP), which collectively show a junctional infiltrate of cytotoxic lymphocytes with liquefaction of the basal layer ("interface dermatitis"). Because recent studies have shown a role for type I interferon (IFN)–associated inflammation, including lymphocyte recruitment via CXCR3 ligand interaction in cutaneous lupus erythematosus and LP, we hypothesized that similar mechanisms might also be involved in liGVHD. Methods Ten representative lesional skin biopsies taken from patients with different subsets of…

Myxovirus Resistance ProteinsChemokinePathologymedicine.medical_specialtyLichenoid EruptionsReceptors CXCR3CD3T-LymphocytesGraft vs Host DiseaseInflammationDermatitisDermatologyIn situ hybridizationCXCR3LigandsChemokine CXCL9Skin DiseasesGTP-Binding ProteinsMedicineCXCL10HumansLymphocytesRNA MessengerIn Situ Hybridizationbiologybusiness.industryLichen PlanusInterferon-alphaChemokine CXCL10stomatognathic diseasesImmunologyChronic DiseaseInterferon Type Ibiology.proteinCXCL9Immunohistochemistrymedicine.symptomEpidermisbusinessJournal of the American Academy of Dermatology
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Cancer cell–autonomous contribution of type I interferon signaling to the efficacy of chemotherapy

2014

International audience; The immune system is routinely confronted with cell death resulting from the physiological turnover of renewable tissues, as well as from pathological insults of several types. We hypothesize the existence of a mechanism that allows the immune system to discriminate between physiological and pathological instances of cell death, but the factors that determine whether cellular demise is perceived as a neutral, tolerogenic or immunogenic event remain unclear 1. Infectious insults are accompanied by so-called microbe-associated molecular patterns (MAMPs), i.e., viral or bacterial products that activate immune cells through a panel of pattern-recognition receptors (PRRs)…

Myxovirus Resistance ProteinsMessengerReceptor Interferon alpha-betaInbred C57BLchemotherapyInterferon alpha-betaMiceInterferonReceptorsAnthracyclinesNeoplasm MetastasisRIG-IPattern recognition receptorAdaptor ProteinsGeneral MedicineNeoadjuvant Therapy3. Good healthGene Expression Regulation NeoplasticTreatment OutcomeReceptors Pattern RecognitionInterferon Type I[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleImmunocompetencemedicine.drugReceptorSignal TransductionBreast Neoplasms[SDV.CAN]Life Sciences [q-bio]/CancerBiologyPattern RecognitionSettore BIO/09General Biochemistry Genetics and Molecular BiologyParacrine signallingImmune systemmedicineCXCL10AnimalsHumanscancerRNA MessengerAutocrine signallingNeoplastic[SDV.IMM.IMM]Life Sciences [q-bio]/Immunology/ImmunotherapyToll-Like Receptor 3Mice Inbred C57BLVesicular TransportChemokine CXCL10Adaptor Proteins Vesicular TransportGene Expression RegulationDoxorubicinImmunologyTLR3RNAAdaptor Proteins Vesicular Transport; Animals; Anthracyclines; Breast Neoplasms; Chemokine CXCL10; Doxorubicin; Female; Gene Expression Regulation Neoplastic; Humans; Immunocompetence; Interferon Type I; Mice Inbred C57BL; Myxovirus Resistance Proteins; Neoadjuvant Therapy; Neoplasm Metastasis; RNA; RNA Messenger; Receptor Interferon alpha-beta; Receptors Pattern Recognition; Toll-Like Receptor 3; Treatment Outcome; Signal Transduction
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Determining a healthy reference range and factors potentially influencing PRO-C3 – A biomarker of liver fibrosis

2021

Background & Aims Progressive fibrosis has been identified as the major predictor of mortality in patients with non-alcoholic fatty liver disease (NAFLD). Several biomarkers are currently being evaluated for their ability to substitute the liver biopsy as the reference standard. Recent clinical studies in NAFLD/NASH patients support the utility of PRO-C3, a marker of type III collagen formation, as a marker for the degree of fibrosis, disease activity, and effect of treatment. Here we establish the healthy reference range, optimal sample handling conditions for both short- and long-term serum storage, and robustness for the PRO-C3 assay. Methods PRO-C3 was measured in 269 healthy volunteers…

NASH-CRN NASH Clinical Research NetworkBiopsyDiseaseAST aspartate aminotransferaseRC799-869Ethnic groupsGastroenterologyNIMBLE Non-Invasive Biomarkers of Metabolic Liver Disease (consortium)FibrosisImmunology and AllergyBody mass indexmedicine.diagnostic_testFatty liverNAS NAFLD Activity ScoreGastroenterologyDiseases of the digestive system. GastroenterologyHospitalsNPV negative predictive valueLiver biopsyBiomarker (medicine)Research Articlemedicine.medical_specialtyNAFLD non-alcoholic fatty liver diseaseADAM A Disintegrin and MetalloproteasesNASH non-alcoholic steatohepatitisReference rangeReference valuesAUROC area under the receiver operating characteristics curveInternal medicineALT alanine aminotransferaseBiopsyInternal MedicinemedicineHumansFIB-4 fibrosis-4Healthy volunteersHepatologyALP alkaline phosphatasebusiness.industryCLSI Clinical and Laboratory Standards InstituteT2DM type 2 diabetes mellitusELF™ test Enhanced Liver Fibrosis testmedicine.diseaseLITMUS Liver Investigation: Testing Marker Utility in Steatohepatitis (consortium)Collagen type IIIFibrosisPPV positive predictive valueReference standardsbusinessBody mass indexBiomarkersNon-alcoholic fatty liver disease
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The genetic contribution of the NO system at the glutamatergic post-synapse to schizophrenia: Further evidence and meta-analysis

2013

NO is a pleiotropic signaling molecule and has an important role in cognition and emotion. In the brain, NO is produced by neuronal nitric oxide synthase (NOS-I, encoded by NOS1) coupled to the NMDA receptor via PDZ interactions; this protein-protein interaction is disrupted upon binding of NOS1 adapter protein (encoded by NOS1AP) to NOS-I. As both NOS1 and NOS1AP were associated with schizophrenia, we here investigated these genes in greater detail by genotyping new samples and conducting a meta-analysis of our own and published data. In doing so, we confirmed association of both genes with schizophrenia and found evidence for their interaction in increasing risk towards disease. Our stron…

NOS1Glutamic AcidNitric Oxide Synthase Type IPolymorphism Single NucleotidePrefrontal cortexNitric oxideAssociationSynapsechemistry.chemical_compoundGlutamatergicSDG 3 - Good Health and Well-beingmedicineAnimalsHumansGenetic Predisposition to DiseasePharmacology (medical)Promoter Regions GeneticPrefrontal cortexBiological PsychiatryAdaptor Proteins Signal TransducingPharmacologyGlutamate receptorComputational BiologyNitric oxideCognitionmedicine.diseasePsychiatry and Mental healthPost-synapseNeurologychemistrySchizophreniaSynapsesRC0321SchizophreniaNeurology (clinical)GlutamatePsychologyRC0321 Neuroscience. Biological psychiatry. NeuropsychiatryNeuroscienceSignal TransductionEuropean Neuropsychopharmacology
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Nalidixic acid-resistant V79 cells with reduced DNA topoisomerase II activity and amplification prone phenotype

1992

Spontaneously nalidixic acid-resistant lines (NAr lines) were selected from a V79 Chinese hamster cell line and phenotypically characterized. NAr lines showed an increased doubling time, a higher number of spontaneous SCE, and more interestingly, decreased DNA topoisomerase II activity. These lines were also cross-resistant to the eukaryotic topoisomerase II inhibitors etoposide and adriamycin, but showed the same level of sensitivity as the parental line to the DNA topoisomerase I inhibitor camptothecin. NAr lines were cross-resistant to other drugs, such as PALA, MTX and MPA, resistance to which has been shown to arise by amplification of the target genes. This last feature, together with…

Nalidixic acidCell SurvivalHealth Toxicology and MutagenesisDrug ResistanceAntineoplastic AgentsBiologyCell LineNalidixic Acidchemistry.chemical_compoundCricetulusCricetinaeGeneticsmedicineAnimalsTopoisomerase II InhibitorsMolecular BiologyGeneEtoposideEtoposideCell NucleusMesocricetusTopoisomeraseGene AmplificationNucleic Acid HybridizationDNADNA topoisomerase II activityMolecular biologyDNA Topoisomerases Type IIPhenotypeDNA Topoisomerases Type IchemistryDoxorubicinbiology.proteinTopoisomerase-II InhibitorSister Chromatid ExchangeDNACamptothecinmedicine.drugMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Oral manifestations of Type I Neurofibromatosis in a family

2011

Neurofibroma is a benign peripheral nerve sheath tumor. It is one of the most frequent tumors of neural origin and its presence is one of the clinical criteria for the diagnosis of neurofibromatosis type I (NF-I). Neurofibromatosis type I is an autosomal dominantly inherited disease due to an alteration in the long arm of chromosome 17. About 50% of NF-I patients have no family history of the disease. NF-I patients have skin lesions (café au lait spots and neurofibromas) as well as bone malformations and central nervous system tumors. Diagnosis is based on a series of clinical criteria. NF-I presents with certain definite oral manifestations which confers to the dentists a major responsibil…

Neurofibromatosis type IPathologymedicine.medical_specialtybusiness.industryOdontologíaDisease:CIENCIAS MÉDICAS [UNESCO]medicine.diseaseCiencias de la saludChromosome 17 (human)Café au lait spotUNESCO::CIENCIAS MÉDICASmedicineNeurofibromaFamily historyNeurofibromatosismedicine.symptombusinessGeneral DentistryPeripheral Nerve SheathJournal of Clinical and Experimental Dentistry
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Adult Neural Stem Cells Are Alerted by Systemic Inflammation through TNF-α Receptor Signaling.

2021

Summary Adult stem cells (SCs) transit between the cell cycle and a poorly defined quiescent state. Single neural SCs (NSCs) with quiescent, primed-for-activation, and activated cell transcriptomes have been obtained from the subependymal zone (SEZ), but the functional regulation of these states under homeostasis is not understood. Here, we develop a multilevel strategy to analyze these NSC states with the aim to uncover signals that regulate their level of quiescence/activation. We show that transitions between states occur in vivo and that activated and primed, but not quiescent, states can be captured and studied in culture. We also show that peripherally induced inflammation promotes a …

NeurogenesisInflammationBiologyReceptors Tumor Necrosis Factor03 medical and health sciences0302 clinical medicineNeural Stem CellsLateral VentriclesGeneticsSubependymal zonemedicineHumansReceptor030304 developmental biologyInflammation0303 health sciencesMicrogliaTumor Necrosis Factor-alphaNeurogenesisCell BiologyNeural stem cellCell biologyAdult Stem Cellsmedicine.anatomical_structurenervous systemReceptors Tumor Necrosis Factor Type IMolecular MedicineSignal transductionmedicine.symptom030217 neurology & neurosurgeryAdult stem cellSignal TransductionCell stem cell
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