Search results for "Nucleases"

showing 10 items of 147 documents

Tree-pollen allergy is efficiently treated by short-term immunotherapy (STI) with seven preseasonal injections of molecular standardized allergens.

1998

The efficacy and tolerance of short-term immunotherapy (STI) by seven preseasonal injections of tree-pollen allergens (ALK7 Fruhbluhermischung) was investigated in a double-blind, placebo-controlled, multicenter study with 111 rhinoconjunctivitis patients. Nasal and bronchial symptoms simultaneously analyzed, and nasal symptoms as a single end point, but not the overall score of nasal, bronchial, and conjunctival symptoms, showed a significantly lower increase with STI during birch-pollen exposure (both P=0.033, n=105, Mann-Whitney U-test). However, a selective analysis with patients from centers with high recruitment figures (n> or =10 patients, n=29 STI, n=32 placebo) showed a significant…

AdultMalemedicine.medical_specialtyAllergyTime FactorsAdolescentmedicine.medical_treatmentImmunologyPlaceboImmunoglobulin Emedicine.disease_causeGastroenterologyInjectionsTreesAllergenRibonucleasesDouble-Blind MethodInternal medicineImmunopathologyotorhinolaryngologic diseasesImmunology and AllergyMedicineHumansDesensitization (medicine)Conjunctivitis AllergicSkin TestsEosinophil cationic proteinbiologybusiness.industryRhinitis Allergic SeasonalBlood Proteinsrespiratory systemAllergensEosinophil Granule ProteinsImmunoglobulin EMiddle Agedmedicine.diseaseClinical trialTreatment OutcomeDesensitization ImmunologicImmunoglobulin GImmunologybiology.proteinPollenFemalebusinessAllergy
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Measurement of inflammatory mediators of eosinophils and lymphocytes in blood in acute asthma: serum levels of ECP influence the bronchodilator respo…

2002

The aim of this study was to assess the relevance of immunoinflammatory markers on the response to short acting β<sub>2</sub>-agonist in acute asthma exacerbation. Thus, we measured serum eosinophil cationic protein (ECP) levels and sIL-2R at acute exacerbation in 52 adult patients with atopic asthma, and assessed forced expiratory volume in 1 s (FEV<sub>1</sub>) before and after the administration of aerosolized salbutamol. After a cumulative dose of salbutamol causing a 10% improvement in FEV<sub>1</sub> from baseline [CD10, i.e. cumulative doses of salbutamol (800 µg) causing an improvement in FEV<sub>1</sub> from baseline to 10%] the patie…

AdultMalemedicine.medical_specialtyExacerbationAdolescentmedicine.drug_classImmunologyStatistics NonparametricRibonucleasesInternal medicineBronchodilatorForced Expiratory VolumemedicineImmunology and AllergyHumansAlbuterolAsthmaSkin TestsEosinophil cationic proteinCumulative dosebusiness.industryReceptors Interleukin-2General MedicineBlood Proteinsrespiratory systemEosinophilAdrenergic beta-AgonistsEosinophil Granule ProteinsImmunoglobulin EMiddle Agedmedicine.diseaseBlood proteinsAsthmarespiratory tract diseasesBronchodilator AgentsEndocrinologymedicine.anatomical_structureImmunologySalbutamolFemalebusinessmedicine.drugInternational archives of allergy and immunology
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The relative roles of intragenic polymorphisms of the vitamin d receptor gene in lumbar spine degeneration and bone density.

2001

Study Design. A retrospective cohort study. Objectives. To compare the magnitudes of the associations of TaqI polymorphisms of the vitamin D receptor gene with bone density and lumbar spine degeneration in the same sample. Summary of Background Data. Vitamin D receptor gene variations are associated with osteoporosis, osteoarthritis, and disc degeneration. Their role in these conditions remains poorly understood. Methods. Bone density of the spine and femur were determined through DEXA, and lumbar disc degeneration was determined from magnetic resonance imaging assessments of signal intensity, disc narrowing, bulging, anular tears, herniations, and osteophytes. Associations between these me…

AdultMalemedicine.medical_specialtyTaqIBone densityGenotypeOsteoporosisPopulationOsteoarthritisCalcitriol receptorCohort StudiesSpinal Osteophytosischemistry.chemical_compoundBone DensityInternal medicineGenotypeOsteoarthritismedicineHumansOrthopedics and Sports MedicineeducationDeoxyribonucleases Type II Site-SpecificIntervertebral DiscAgedRetrospective Studieseducation.field_of_studyLumbar VertebraePolymorphism Geneticbusiness.industryMiddle Agedmedicine.diseaseEndocrinologychemistryTearsOsteoporosisReceptors CalcitriolTwin Studies as TopicFemaleNeurology (clinical)businessIntervertebral Disc DisplacementSpine
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SNPs and taxane toxicity in breast cancer patients

2014

Aim: In order to identify genetic variants associated with taxanes toxicity, a panel with 47 SNPs in 20 genes involved in taxane pathways was designed. Patients & methods: Genomic DNA of 113 breast cancer patients was analyzed (70 taking docetaxel, 43 taking paclitaxel). Results: Two SNPs associated with docetaxel toxicity were identified: CYP3A4*1B with infusion-related reactions; and ERCC1 Gln504Lys with mucositis (p ≤ 0.01). Regarding paclitaxel toxicity: CYP2C8 HapC and CYP2C8 rs1934951 were associated with anemia; and ERCC1 Gln504Lys with neuropathy (p ≤ 0.01). Conclusion: Genes involved in DNA repair mechanisms and reactive oxygen species levels influence taxane toxicity in cance…

Bridged-Ring CompoundsMucositisOncologymedicine.medical_specialtyDrug-Related Side Effects and Adverse ReactionsPaclitaxelmedicine.medical_treatmentBreast NeoplasmsDocetaxelPharmacologyPolymorphism Single Nucleotidechemistry.chemical_compoundBreast cancerInternal medicineGeneticsMucositisCytochrome P-450 CYP3AHumansMedicineGenetic Association StudiesAgedPharmacologyChemotherapyTaxanebusiness.industryCancerMiddle AgedEndonucleasesmedicine.diseaseDNA-Binding ProteinsDocetaxelPaclitaxelchemistryMolecular MedicineFemaleTaxoidsERCC1businessmedicine.drugPharmacogenomics
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CtIP silencing as a novel mechanism of tamoxifen resistance in breast cancer.

2007

AbstractAcquired resistance to the antiestrogen tamoxifen constitutes a major clinical challenge in breast cancer therapy. However, the mechanisms involved are still poorly understood. Using serial analysis of gene expression, we identified CtIP, a BRCA1- and CtBP-interacting protein, as one of the most significantly down-regulated transcripts in estrogen receptor α–positive (ER+) MCF-7 tamoxifen-resistant breast cancer cells. We further confirmed the association of CtIP down-regulation with tamoxifen resistance in an additional ER+ breast cancer line (T47D), strengthening the relevance of the phenomenon observed. In additional studies, we found CtIP protein expression in a majority of ER+ …

Cancer ResearchAntineoplastic Agents HormonalEstrogen receptorDown-RegulationBreast NeoplasmsDisease-Free SurvivalBreast cancerCell Line TumormedicineGene silencingHumansSerial analysis of gene expressionGene Silencingskin and connective tissue diseasesMolecular BiologyEndodeoxyribonucleasesbusiness.industryCancerNuclear ProteinsAntiestrogenmedicine.diseaseGrowth InhibitorsGene Expression Regulation NeoplasticTamoxifenOncologyDrug Resistance NeoplasmCancer researchFemalebusinessCarrier ProteinsTamoxifenProgressive diseasemedicine.drugMolecular cancer research : MCR
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Antitumor effect of B16 melanoma cells genetically modified with the angiogenesis inhibitor rnasin.

2001

The growth of new blood vessels is an essential condition for the development of tumors with a diameter greater than 1-2 mm and also for their metastatic dissemination. RNasin, the placental ribonuclease inhibitor, is known to have antiangiogenic activity through the inhibition of angiogenin and basic fibroblast growth factor. Nevertheless, the administration of the recombinant form of a protein poses several limitations; as a result, we have studied the antitumor effect of RNasin in a murine gene therapy model. RNasin cDNA was subcloned into the pcDNA3 expression vector, and the resulting recombinant plasmid was used to transfect the B16 murine melanoma cell line. An RNasin inverted constr…

Cancer ResearchLung NeoplasmsAngiogeninTranscription GeneticGenetic enhancementCellBasic fibroblast growth factorGenetic VectorsMelanoma ExperimentalGene ExpressionAngiogenesis InhibitorsTransfectionNeovascularizationImmunoenzyme Techniqueschemistry.chemical_compoundMiceRibonucleasesmedicineTumor Cells CulturedAnimalsHumansRNA MessengerEnzyme InhibitorsMolecular BiologyDNA PrimersNeovascularization PathologicReverse Transcriptase Polymerase Chain ReactionMelanomaGenetic Therapymedicine.diseaseAngiogenesis inhibitormedicine.anatomical_structurechemistryCell cultureCancer researchMolecular Medicinemedicine.symptomPlacental HormonesCell DivisionCancer gene therapy
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Bovine seminal ribonuclease is cytotoxic for both malignant and normal telomerase-positive cells

2005

Bovine seminal-ribonuclease (BS-RNase) is a member of the 'ribonucleases with special biological actions' family since it possesses specific anti-tumour, anti-spermatogenic and embryotoxic activities and exerts an immunosuppressive effect on T lymphocytes. In previous studies it was demonstrated that BS-RNase induced apoptosis in proliferating, malignant and normal cells and that telomerase activity loss also caused apoptotic death in neoplastic cells. Since an obvious relationship between cell proliferation and telomerase activity exists, the aim of this work was to study if the pro-apoptotic cytotoxic action exerted by BS-RNase on proliferating malignant cells (HT29) and proliferating nor…

Cancer ResearchTelomeraseTime FactorsT-LymphocytesCellular differentiationCytotoxicityBlotting WesternDown-RegulationTetrazolium SaltsAntineoplastic AgentsApoptosisEnzyme-Linked Immunosorbent AssayBiologyHT29 CellsCell Line TumorEndoribonucleasesAnimalsHumansCytotoxic T cellTelomerase reverse transcriptaseLymphocytesRNA MessengerTelomeraseBovine seminal-ribonuclease; Cytotoxicity; HTR; Nucleolar localization; TelomeraseCell ProliferationReverse Transcriptase Polymerase Chain ReactionCell growthCell DifferentiationCell cycleNucleolar localizationMolecular biologyThiazolesBovine seminal-ribonucleaseMicroscopy FluorescenceOncologyCell cultureLeukocytes MononuclearMicroscopy Electron ScanningRNACattleHTRCell NucleolusImmunosuppressive Agents
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TFIIH Operates through an Expanded Proximal Promoter To Fine-Tune c-myc Expression

2004

A continuous stream of activating and repressing signals is processed by the transcription complex paused at the promoter of the c-myc proto-oncogene. The general transcription factor IIH (TFIIH) is held at promoters prior to promoter escape and so is well situated to channel the input of activators and repressors to modulate c-myc expression. We have compared cells expressing only a mutated p89 (xeroderma pigmentosum complementation group B [XPB]), the largest TFIIH subunit, with the same cells functionally complemented with the wild-type protein (XPB/wt-p89). Here, we show structural, compositional, and functional differences in transcription complexes between XPB and XPB/wt-89 cells at t…

Chromatin ImmunoprecipitationDNA ComplementaryCell SurvivalUltraviolet RaysBlotting WesternGreen Fluorescent ProteinsGene ExpressionRepressorCellular homeostasisBiologyTransfectionModels BiologicalProto-Oncogene MasProto-Oncogene Proteins c-mycTranscription Factors TFIIRibonucleasesPotassium PermanganateTranscription (biology)HumansRNA MessengerPromoter Regions GeneticMolecular BiologyModels GeneticGeneral transcription factorCell CycleGenetic Complementation TestDNA HelicasesPromoterCell BiologyFibroblastsFlow CytometryMolecular biologyDNA-Binding ProteinsKineticsTranscription Factor TFIIHMicroscopy FluorescenceMutationTranscription preinitiation complexTranscription factor II HTranscription Factor TFIIHPlasmidsMolecular and Cellular Biology
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Covalent DNA adducts formed by benzo[c]chrysene in mouse epidermis and by benzo[c]chrysene fjord-region diol epoxides reacted with DNA and polynucleo…

1997

The metabolic activation in mouse skin of benzo[c]chrysene (B[c]C), a weakly carcinogenic polycyclic aromatic hydrocarbon (PAH) present in coal tar and crude oil, was investigated. Male Parkes mice were treated topically with 0.5 mumol of B[c]C, and DNA was isolated from the treated areas of skin at various times after treatment and analyzed by 32P-postlabeling. Seven adduct spots were detected, at a maximum level of 0.89 fmol of adducts/microgram of DNA. Four B[c]C-DNA adducts persisted in skin for at least 3 weeks. Treatment of mice with 0.5 mumol of the optically pure putative proximate carcinogens (+)- and (-)-trans-benzo[c]chrysene-9,10-dihydrodiols [(+)- and (-)-B[c]C-diols] led to th…

ChryseneMaleStereochemistryPolynucleotidesToxicologyAdductchemistry.chemical_compoundDNA AdductsMiceAnimalsCarcinogenBiotransformationChromatography High Pressure LiquidSkinCarcinogenic Polycyclic Aromatic HydrocarbonSingle-Strand Specific DNA and RNA EndonucleasesAbsolute configurationGeneral MedicineDNAPhenanthreneschemistryCovalent bondPolynucleotideAutoradiographyEpoxy CompoundsSpectrophotometry UltravioletChromatography Thin LayerDNAChemical research in toxicology
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Benzo[a]pyrene represses DNA repair through altered E2F1/E2F4 function marking an early event in DNA damage-induced cellular senescence

2020

AbstractTranscriptional regulation of DNA repair is of outmost importance for the restoration of DNA integrity upon genotoxic stress. Here we report that the potent environmental carcinogen benzo[a]pyrene (B[a]P) activates a cellular DNA damage response resulting in transcriptional repression of mismatch repair (MMR) genes (MSH2, MSH6, EXO1) and of RAD51, the central homologous recombination repair (HR) component, ultimately leading to downregulation of MMR and HR. B[a]P-induced gene repression is caused by abrogated E2F1 signalling. This occurs through proteasomal degradation of E2F1 in G2-arrested cells and downregulation of E2F1 mRNA expression in G1-arrested cells. Repression of E2F1-me…

Cyclin-Dependent Kinase Inhibitor p21SenescenceAcademicSubjects/SCI00010DNA repairDNA damageRAD51E2F4 Transcription FactorBiologyDNA Mismatch Repair03 medical and health sciences0302 clinical medicineCell Line TumorBenzo(a)pyreneGeneticsHumansCellular SenescenceCell Line Transformed030304 developmental biology0303 health sciencesGene regulation Chromatin and EpigeneticsRecombinational DNA RepairEpithelial CellsKv Channel-Interacting ProteinsCell Cycle CheckpointsDNAFibroblastsCell biologyDNA-Binding ProteinsRepressor ProteinsMSH6DNA Repair EnzymesExodeoxyribonucleasesMutS Homolog 2 ProteinGamma RaysMSH2030220 oncology & carcinogenesisCarcinogensMCF-7 CellsDNA mismatch repairRad51 RecombinaseCell agingE2F1 Transcription FactorDNA DamageSignal TransductionNucleic Acids Research
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