Search results for " sequence"

showing 10 items of 3643 documents

Expression of properdin in human monocytes

1994

Properdin is the only known positive regulator of the alternative pathway of complement activation. Northern blot analysis of cell lines derived from fibroblasts, B-cells, hepatoma cells, and cells of the monocyte-macrophage lineage revealed properdin expression only in the myelomonocytic cell line HL-60, in the monoblastic cell line U-937 and in the monocytic line Mono Mac 6. Culture of Mono Mac 6 cells for 24 h with phorbol 12-myristate 13-acetate, bacterial lipopolysaccharide and the cytokines interleukin-1 beta and tumour necrosis factor-alpha enhanced mRNA abundance, with the strongest effect (tenfold) being observed with the lipopolysaccharide. In contrast, recombinant interferon-gamm…

AdultLipopolysaccharidesLipopolysaccharidemedicine.medical_treatmentMolecular Sequence DataEnzyme-Linked Immunosorbent AssayBiologyurologic and male genital diseasesBiochemistryMonocytesCell LineInterferon-gammachemistry.chemical_compoundTumor Cells CulturedmedicineHumansRNA MessengerNorthern blotBase SequenceProperdinTumor Necrosis Factor-alphaMacrophagesMonocyteBlotting NorthernMolecular biologyRecombinant ProteinsComplement systemCytokinemedicine.anatomical_structurechemistryCell cultureImmunologyAlternative complement pathwayCytokinesTetradecanoylphorbol AcetateProperdinInterleukin-1European Journal of Biochemistry
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HCV viraemia is more important than genotype as a predictor of response to interferon in sicily (Southern Italy)

1996

Abstract Background/Aims: To investigate host- and virus-related factors predictive of early and sustained alanine aminotransferase normalization after interferon therapy for HCV-related chronic liver disease, in an area where genotype 1 is highly prevalent. Methods: We studied 100 patients with HCV-RNA positive chronic liver disease (73 chronic hepatitis and 27 cirrhosis) undergoing alpha-interferon treatment. Thirty-four patients had an early response but relapsed, 15 patients remained into sustained response for at least 12 months after therapy, and 51 patients did not respond. Serum HCV-RNA levels were assessed by bDNA (Chiron), and genotype by LiPA (Innogenetics) and by sequencing of t…

AdultLiver CirrhosisMaleCirrhosisGenotypeHepatitis C virusMolecular Sequence DataAlpha interferonChronic liver diseasemedicine.disease_causeAntiviral AgentsGenotypePrevalenceBDNA testmedicineHumansViremiaSicilyInterferon alfaBase SequenceHepatologybusiness.industryInterferon-alphaAlanine TransaminaseHepatitis CMiddle Agedmedicine.diseaseHepatitis CTreatment OutcomeLiverChronic DiseaseImmunologyNucleic Acid ConformationFemalebusinessmedicine.drugJournal of Hepatology
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The impact of virus population diversity on the dynamics of cytomegalovirus DNAemia in allogeneic stem cell transplant recipients

2017

Mixed cytomegalovirus (CMV) infections are associated with delayed viral clearance in solid organ transplant recipients. We investigated whether this could be extrapolated to allogeneic stem cell transplant (allo-SCT) recipients. A total of 48 plasma specimens, obtained during 29 episodes of active CMV infection in 25 non-consecutive allo-SCT patients, were analysed. Baseline blood specimens, drawn shortly prior to the inception of pre-emptive antiviral therapy (pre-treatment specimen; n=29), as well as follow-up samples obtained either after the initiation of antiviral therapy (post-treatment specimen; n=15) or during recurrent episodes (n=4) were analysed. Plasma CMV DNA loads were quanti…

AdultMale0301 basic medicine030106 microbiologyCytomegalovirusBiologymedicine.disease_causeAntiviral AgentsVirus03 medical and health sciencesVirologyGenotypemedicineHumansTransplantation HomologousGenotypingAgedBase SequenceGenetic VariationHigh-Throughput Nucleotide Sequencingvirus diseasesCytomegalovirusSequence Analysis DNACmv dnaemiaMiddle AgedViral LoadVirologyHypervariable region030104 developmental biologyCytomegalovirus InfectionsDNA ViralImmunologyFemalePopulation diversityStem cellStem Cell TransplantationJournal of General Virology
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Quizartinib versus salvage chemotherapy in relapsed or refractory FLT3-ITD acute myeloid leukaemia (QuANTUM-R): a multicentre, randomised, controlled…

2019

Background Patients with relapsed or refractory FLT3 internal tandem duplication (FLT3-ITD)-positive acute myeloid leukaemia have a poor prognosis, including high frequency of relapse, poorer response to salvage therapy, and shorter overall survival than those with FLT3 wild-type disease. We aimed to assess whether single-agent quizartinib, an oral, highly potent and selective type II FLT3 inhibitor, improves overall survival versus salvage chemotherapy. Methods QuANTUM-R is a randomised, controlled, phase 3 trial done at 152 hospitals and cancer centres in 19 countries. Eligible patients aged 18 years or older with ECOG performance status 0-2 with relapsed or refractory (duration of first …

AdultMale0301 basic medicinemedicine.medical_specialtyPopulationSalvage therapy/Gastroenterology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicinemedicineHumansBenzothiazoleseducationSurvival rateAgedQuizartinibSalvage Therapyeducation.field_of_studybusiness.industryPhenylurea CompoundsMiddle Agedmedicine.diseaseFludarabineSurvival RateTransplantationLeukemia Myeloid AcuteSettore MED/15 - MALATTIE DEL SANGUE030104 developmental biologyfms-Like Tyrosine Kinase 3OncologychemistryTandem Repeat Sequences030220 oncology & carcinogenesisCytarabineFemaleNeoplasm Recurrence LocalbusinessFebrile neutropeniamedicine.drug
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PORCN mutations in focal dermal hypoplasia: coping with lethality.

2009

Contains fulltext : 81709.pdf (Publisher’s version ) (Closed access) The X-linked dominant trait focal dermal hypoplasia (FDH, Goltz syndrome) is a developmental defect with focal distribution of affected tissues due to a block of Wnt signal transmission from cells carrying a detrimental PORCN mutation on an active X-chromosome. Molecular characterization of 24 unrelated patients from different ethnic backgrounds revealed 23 different mutations of the PORCN gene in Xp11.23. Three were microdeletions eliminating PORCN and encompassing neighboring genes such as EBP, the gene associated with Conradi-Hunermann-Happle syndrome (CDPX2). 12/24 patients carried nonsense mutations resulting in loss …

AdultMaleAdolescentBase SequenceDNA Mutational AnalysisMolecular Sequence DataInfant NewbornInfantMembrane ProteinsGenomic disorders and inherited multi-system disorders [IGMD 3]Focal Dermal HypoplasiaSettore MED/38 - Pediatria Generale E SpecialisticaSettore MED/03 - Genetica MedicaChild PreschoolMutationGoltz syndrome FDH PORCN WNT skewed X-inactivation postzygotic mosaicHumansProtein IsoformsFemaleAmino Acid SequenceChildAcyltransferasesHuman Mutation
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Characterization of 14 novel deletions underlying Rubinstein–Taybi syndrome: an update of the CREBBP deletion repertoire

2015

Rubinstein–Taybi syndrome (RSTS) is a rare, clinically heterogeneous disorder characterized by cognitive impairment and several multiple congenital anomalies. The syndrome is caused by almost private point mutations in the CREBBP (~55 % of cases) and EP300 (~8 %) genes. The CREBBP mutational spectrum is variegated and characterized by point mutations (30–50 %) and deletions (~10 %). The latter are diverse in size and genomic position and remove either the whole CREBBP gene and its flanking regions or only an intragenic portion. Here, we report 14 novel CREBBP deletions ranging from single exons to the whole gene and flanking regions which were identified by applying complementary cytomolecu…

AdultMaleAdolescentContiguous gene syndromeCohort StudiesExonGeneticmedicineGeneticsHumansPoint MutationCREB-binding proteinEP300ChildPreschoolGenetics (clinical)Sequence DeletionGeneticsRubinstein-Taybi Syndromebiologymedicine.diagnostic_testRubinstein–Taybi syndromeBase SequencePoint mutationMedicine (all)Infant NewbornInfantMiddle Agedmedicine.diseaseNewbornCREB-Binding ProteinHuman geneticsAdolescent; Adult; CREB-Binding Protein; Child; Child Preschool; Cohort Studies; Female; Humans; Infant; Infant Newborn; Male; Middle Aged; Rubinstein-Taybi Syndrome; Base Sequence; Point Mutation; Sequence Deletion; Genetics (clinical); Genetics; Medicine (all)Child Preschoolbiology.proteinFemaleCohort StudieAdolescent; Adult; CREB-Binding Protein; Child; Child Preschool; Cohort Studies; Female; Humans; Infant; Infant Newborn; Male; Middle Aged; Rubinstein-Taybi Syndrome; Base Sequence; Point Mutation; Sequence Deletion; Medicine (all); Genetics; Genetics (clinical)Fluorescence in situ hybridizationHuman
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Histone acetylation deficits in lymphoblastoid cell lines from patients with Rubinstein-Taybi syndrome.

2012

Background: Rubinstein-Taybi syndrome (RSTS) is a congenital neurodevelopmental disorder defined by postnatal growth deficiency, characteristic skeletal abnormalities and mental retardation and caused by mutations in the genes encoding for the transcriptional co-activators with intrinsic lysine acetyltransferase (KAT) activity CBP and p300. Previous studies have shown that neuronal histone acetylation is reduced in mouse models of RSTS. Methods: The authors identified different mutations at the CREBBP locus and generated lymphoblastoid cell lines derived from nine patients with RSTS carrying distinct CREBBP mutations that illustrate different grades of the clinical severity in the spectrum …

AdultMaleAdolescentDNA Mutational AnalysisGene ExpressionHaploinsufficiencyHydroxamic AcidsHistone DeacetylasesHistonesNeurodevelopmental disorderSettore MED/38 - Pediatria Generale E SpecialisticaHistone H2AGeneticsmedicineHistone H2BHumansCREBBP geneChildGeneGenetics (clinical)Cell Line TransformedRubinstein-Taybi SyndromebiologyRubinstein–Taybi syndromeBase SequenceAcetylationmedicine.diseaseMolecular biologyCREB-Binding ProteinChromatinHistone Deacetylase InhibitorsHistoneSettore MED/03 - Genetica MedicaAcetylationChild PreschoolMutationbiology.proteinCancer researchLeukocytes MononuclearFemaleHaploinsufficiencyE1A-Associated p300 ProteinBiomarkersJournal of medical genetics
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LKM-1 autoantibodies recognize a short linear sequence in P450IID6, a cytochrome P-450 monooxygenase.

1991

LKM-1 autoantibodies, which are associated with autoimmune chronic active hepatitis, recognize P450IID6, a cytochrome P-450 monooxygenase. The reactivities of 26 LKM-1 antisera were tested with a panel of deletion mutants of P450IID6 expressed in Escherichia coli. 22 sera recognize a 33-amino acid segment of P450IID6, and 11 of these recognize a shorter segment, DPAQPPRD. PAQPPR is also found in IE175 of herpes simplex virus type 1 (HSV-1). Antibodies for HSV-1 proteins were detected by ELISA in 17 of 20 LKM-1 sera tested. An immobilized, synthetic peptide, DPAQPPRDC, was used to purify LKM-1 antibodies. Affinity purified LKM-1 autoantibodies react on immunoblots with a protein in BHK cells…

AdultMaleAdolescentHepatitis C virusMolecular Sequence DataHepacivirusmedicine.disease_causeAntibodies ViralEpitopeAutoimmune DiseasesEpitopesViral ProteinsCytochrome P-450 Enzyme SystemmedicineHumansSimplexvirusAmino Acid SequencePeptide sequenceAutoantibodiesHepatitis ChronicAntiserumbiologyAutoantibodyGeneral MedicineMonooxygenaseMiddle AgedVirologyHerpes simplex virusbiology.proteinOxygenasesFemaleAntibodyResearch ArticleThe Journal of clinical investigation
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Mutation analysis in myophosphorylase deficiency (McArdle's disease).

1998

Inherited deficiency of myophosphorylase leads to glycogen storage disease type V (McArdle's disease). We performed mutation analysis in 9 patients of eight unrelated families from Germany with typical cliniclal presentation of myophos-phorylase deficiency. Beside previously described mutations we identified four novel mutations in the myophorsphorylase gene. Four patients were homozygous for a nonsense mutation Arg49Stop that has been reported to be the most common mutation in white patients. Two affected siblings were compound heterozygotes for a novel missense mutation Gly685Arg and the nonsense mutation Arg49Stop. One patient carried a novel nonsense mutation Arg575Stop and a previously…

AdultMaleAdolescentNonsense mutationDNA Mutational AnalysisBiologyCompound heterozygosityPolymerase Chain ReactionmedicineMissense mutationHumansAmino Acid SequenceChildCodonAgedGeneticsTransition (genetics)Base SequenceHomozygoteMiddle Agedmedicine.diseaseNeurologyMyophosphorylaseMutation (genetic algorithm)MutationMutation testingGlycogen Storage Disease Type VFemaleNeurology (clinical)Glycogen storage disease type VPolymorphism Restriction Fragment LengthAnnals of neurology
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Single-Nucleotide Polymorphism Array-Based Characterization of Ring Chromosome 18

2012

Objective To study genotype–phenotype correlation of ring chromosome 18 [r(18)] in 9 patients with 46,XN karyotype. Study design In 9 patients with a de novo 46,XN,r(18) karyotype (7 females, 2 males), we performed high-resolution single-nucleotide polymorphism array analysis (Illumina Human Omni1-QuadV1 array in 6 patients, Affymetrix 6.0 array in 3 patients), investigation of parental origin, and genotype–phenotype correlation. Results No breakpoint was recurrent. Single metaphases with loss of the ring, double rings, or secondarily rearranged rings were found in some cases, but true mosaicism was present in none of these cases. In 3 patients, additional duplications in 18p (of 1.4 Mb, 2 …

AdultMaleAdolescentRing chromosomeSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideCROMOSSOMOS HUMANOS (ANORMALIDADES;COMPLICAÇÕES)Young AdultMeiosisPolymorphism (computer science)SNPBody SizeHumansRing ChromosomesChildGenetic Association StudiesOligonucleotide Array Sequence AnalysisGeneticsBreakpointInfant NewbornInfantKaryotypeMiddle AgedPhenotypeChild PreschoolKaryotypingPediatrics Perinatology and Child HealthFemaleChromosome DeletionChromosomes Human Pair 18HeadMaternal AgeMicrosatellite Repeats
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