Search results for " Single-Stranded"

showing 10 items of 81 documents

Increasing rates of DNA single-strand breaks in lymphocytes of clinical personnel handling cytostatic drugs

1993

A total of 27 persons, working in cancer stations with exposure to cytostatics, and 40 healthy control persons were examined for DNA single-strand breaks in peripheral lymphocytes. Non-smoking personnel from cancer stations were found to have an increased rate of DNA single-strand breaks compared to the non-smoking control subjects. In the case of smokers an increased rate of DNA single-strand breaks could be recorded for those working in cancer stations as well as with the controls. DNA single-strand breaks indicate reversible damage to DNA. As DNA repair is not perfect in every case, an increased number of DNA single-strand breaks leads to irreversible DNA damage.

AdultMaleCancer Researchmedicine.medical_specialtyDNA damageDNA repairLymphocyteDNA Single-StrandedAntineoplastic AgentsBiologyMedical Oncologychemistry.chemical_compoundInternal medicinemedicineHumansLymphocytesGeneticsDNA single strandHematologyCancerGeneral MedicineMiddle Agedmedicine.diseasePersonnel Hospitalmedicine.anatomical_structureOncologychemistryToxicityCancer researchFemaleDNADNA DamageJournal of Cancer Research and Clinical Oncology
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Cholinesterase variants: rapid characterisation by PCR/SSCP and evidence for molecular homogeneity.

1995

We have applied the technique of PCR-SSCP (polymerase chain reaction-single stranded conformation polymorphism) to characterise the molecular basis of cholinesterase deficiency and variants in a Jordanian family. PCR-SSCP proved to be a quick and sensitive method of screening cholinesterase variants in a clinical setting. An AG insertion at position 351 was found to cause a silent allele, for which the parents were heterozygous and three children homozygous. In addition, the father and two sons were heterozygous for an A to G transition at position 209, known to cause the dibucaine resistant variant. No linkage to the K variant was found, which has been reported previously in white populati…

AdultMaleGenotypeGenetic LinkageMolecular Sequence DataDibucainePolymerase Chain ReactionFrameshift mutationlaw.inventionlawGenetic linkageGenotypeGeneticsCholinesterasesHumansPoint MutationGenetic TestingAlleleFrameshift MutationGenetics (clinical)PolymerasePolymerase chain reactionAllelesPolymorphism Single-Stranded ConformationalCholinesteraseGeneticsJordanbiologyBase SequencePoint mutationSequence Analysis DNAMolecular biologyPedigreebiology.proteinFemaleMetabolism Inborn ErrorsResearch ArticleJournal of medical genetics
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Serum hepatitis C virus (HCV)-RNA and response to alpha-interferon in anti-HCV positive chronic hepatitis

1992

Hepatitis C virus (HCV) replication was assessed before and during alpha-interferon (IFN) treatment in 22 anti-HCV positive patients with posttransfusion or sporadic chronic hepatitis (CH). Eleven patients were “responders” and 11 patients “non-responders” to IFN. Thirteen anti-HCV negative healthy subjects and five anti-HCV negative patients with autoimmune CH served as controls. Serum HCV-RNA was detected by the polymerase chain reaction (PCR) in all untreated anti-HCV positive patients but in none of the anti-HCV negative subjects. PCR primers from the 5′-non-coding (NC) region were more sensitive than primers from a non-structural (NS5) region in detecting HCV-RNA (21/22, 95% vs. 7/22, …

AdultMaleHepatitis C virusMolecular Sequence DataDNA Single-StrandedAlpha interferonHepacivirusAutoimmune hepatitisInterferon alpha-2Virus Replicationmedicine.disease_causePolymerase Chain ReactionSensitivity and SpecificityVirusInterferonVirologymedicineHumansHepatitis AntibodiesViremiaBase Sequencebiologybusiness.industryInterferon-alphavirus diseasesHepatitis C AntibodiesMiddle Agedmedicine.diseaseHepatitis CVirologyRecombinant ProteinsTiterInfectious DiseasesChronic DiseaseImmunologybiology.proteinRNA ViralFemaleViral diseaseAntibodybusinessmedicine.drugJournal of Medical Virology
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Characterization of non-expressed C4 genes in a case of complete C4 deficiency: identification of a novel point mutation leading to a premature stop …

1998

The genetic basis of complete C4 deficiency in a patient with SLE was investigated. Previous studies have demonstrated that this patient has two different major histocompatibility complex (MHC) haplotypes that each contain a major deletion and a non-expressed C4 gene. In the present study, non-expression of the C4 genes was explained by the finding of two distinct C4 gene mutations. A previously described two base pair insertion in exon 29 of the C4 gene was detected in the paternal MHC haplotype [HLA-A2, B40, SC00, DR6]. The maternal haplotype [HLA-A30, B18, F1C00, DR3] carried a C4 gene with a one base pair deletion in exon 20 generating a premature stop codon. This mutation was neither f…

AdultMaleHeterozygoteImmunologyGene mutationBiologymedicine.disease_causePolymerase Chain ReactionCell LineMajor Histocompatibility ComplexExonmedicineImmunology and AllergyHumansLupus Erythematosus SystemicPoint MutationGenePolymorphism Single-Stranded ConformationalGeneticsMutationPoint mutationHaplotypeC4AComplement C4General MedicineExonsSequence Analysis DNAMolecular biologyIsotypePedigreeHaplotypesCodon TerminatorFemalePolymorphism Restriction Fragment LengthHuman immunology
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Evaluation of clinical diagnosis criteria of familial ligand defective apoB 100 and lipoprotein phenotype comparison between LDL receptor gene mutati…

2007

Familial hypercholesterolemia (FH) and familial defective apoB 100 (FDB) are characterized by increased plasma low-density lipoprotein cholesterol (LDLc) levels and risk of coronary heart disease (CHD). FDB is clinically indistinguishable from FH. The aims of this study were to evaluate clinical diagnosis criteria for FDB and to compare the lipoprotein phenotype between carriers of LDL receptor (LDLR) gene mutations that affect the ligand-binding domain and subjects with the R3500Q mutation in apoB gene. We studied 213 subjects (113 probands) with FH and 19 heterozygous FDB subjects. Genetic diagnosis was determined by following a protocol based on Southern blot and polymerase chain reactio…

AdultMaleHeterozygotemedicine.medical_specialtyGenotypeApolipoprotein BPopulationMutation MissenseCoronary DiseaseFamilial hypercholesterolemiaGene mutationBiologyWhite PeopleHyperlipoproteinemia Type IIchemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineHumansMissense mutationeducationPolymorphism Single-Stranded Conformationaleducation.field_of_studyBinding SitesCholesterolGenetic Carrier ScreeningBiochemistry (medical)Public Health Environmental and Occupational HealthCholesterol LDLGeneral MedicineMiddle Agedmedicine.diseaseFounder EffectProtein Structure TertiaryEuropePhenotypeEndocrinologyReceptors LDLchemistryApolipoprotein B-100LDL receptorbiology.proteinFemalelipids (amino acids peptides and proteins)LipoproteinTranslational Research
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Molecular analysis of the erythropoietin receptor system in patients with polycythaemia vera

1994

Summary Erythropoietin (EPO) is a potent regulator of the viability, proliferation and differentiation of erythroid progenitor cells. Its effect is mediated by binding to the erythropoietin receptor (EPO-R), a member of a new cytokine receptor family. Alterations of the EPO/EPO-R system have recently been shown to be involved in the pathogenesis of familial erythrocytosis and polycythaemia vera (PV). In order to define whether genetic changes in the EPO-R gene and its ligand play a role in the development of PV, the structure and expression levels of the EPO-R and EPO genes were examined in samples from bone marrow and/or peripheral blood mononuclear cells of 24 patients with PV. As expecte…

AdultMalePolycythaemiaTranscription GeneticMolecular Sequence DataBiologyPolymerase Chain ReactionPeripheral blood mononuclear cellPolycythemia veraBone Marrowhemic and lymphatic diseasesReceptors ErythropoietinmedicineHumansRNA MessengerErythropoietinPolycythemia VeraPolymorphism Single-Stranded ConformationalAgedBase SequenceHematologyMiddle Agedmedicine.diseaseMolecular biologyReverse transcriptaseErythropoietin receptormedicine.anatomical_structureErythropoietinFemaleBone marrowOligonucleotide ProbesCytokine receptormedicine.drugBritish Journal of Haematology
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Ten novel mutations found in Aniridia.

1998

Aniridia (AN) is a sight-threatening congenital ocular disorder characterized by iris hypoplasia, corneal pannus, foveal and optic nerve hypoplasia, cataract formation, and glaucoma. In two-thirds of the patients, AN is inherited in an autosomal dominant fashion with almost complete penetrance but variable expression. The remaining cases are sporadic. Aniridia has been shown to be associated with mutations in the PAX6 gene, located on chromosome 11p13, telomeric to the Wilms' tumor predisposition gene (WT1). This paper describes 14 mutations in the PAX6 gene in patients with AN. Among these 14 mutations, 10 have been unpublished until now. They result most probably in haploinsufficiency and…

AdultMalegenetic structuresAdolescentPAX6 Transcription FactorDNA Mutational AnalysisMolecular Sequence DataBiologyPolymerase Chain ReactionVariable ExpressionGeneticsmedicineHumansPaired Box Transcription FactorsAmino Acid SequenceChildEye ProteinsGeneAniridiaGenetics (clinical)Polymorphism Single-Stranded ConformationalGeneticsHomeodomain ProteinsOptic nerve hypoplasiaInfantMiddle Agedmedicine.diseasePenetranceeye diseasesDNA-Binding ProteinsRepressor ProteinsAniridiaChild PreschoolMutationHomeoboxFemalesense organsPAX6HaploinsufficiencyTranscription FactorsHuman mutation
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Search for variants of the gene-promoter and the potential phosphotyrosine encoding sequence of the insulin receptor substrate-2 gene: evaluation of …

1999

Aims/hypothesis. The aim of this study was to screen part of the putative promoter sequence in addition to 14 potential phosphotyrosine residues of human IRS-2 for genetic variability which might cause changes in protein expression or function. Furthermore, the potential impact on insulin secretion and sensitivity of a previously identified IRS-2 variant (Gly1057Asp) was analysed Methods. The screenings were carried out by the SSCP-heteroduplex technique on DNA from Type II (non-insulin-dependent) diabetic patients. The impact of the Gly1057Asp variant was analysed in four glucose-tolerant Scandinavian study groups. Results. The results showed no nucleotide substitutions in the promoter seq…

AdultMalemedicine.medical_specialtyAdolescentInsulin Receptor Substrate ProteinsEndocrinology Diabetes and Metabolismmedicine.medical_treatmentMolecular Sequence Datamedicine.disease_causeGene FrequencyTwo-Hybrid System TechniquesInternal medicineDiabetes mellitusInsulin SecretionInternal MedicinemedicineHumansInsulinGenetic TestingProspective StudiesPhosphotyrosinePromoter Regions GeneticPolymorphism Single-Stranded ConformationalPancreatic hormoneAgedMutationGlucose tolerance testBase Sequencebiologymedicine.diagnostic_testGenetic Carrier ScreeningInsulinIntracellular Signaling Peptides and ProteinsGlucose Tolerance TestMiddle AgedPhosphoproteinsmedicine.diseaseIRS2PedigreeInsulin receptorEndocrinologyAmino Acid SubstitutionDiabetes Mellitus Type 2Insulin Receptor Substrate Proteinsbiology.proteinDiabetologia
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Association of C677T polymorphism in MTHFR gene, high homocysteine and low HDL cholesterol plasma values in heterozygous familial hypercholesterolemi…

2010

Aim: to investigate the association of C677T polymorphism in the methylene tetrahydrofolate reductase (MTHFR) gene, homocysteine plasma values (Hcy), and plasma HDL cholesterol in heterozy-gous familial hypercholesterolemia (hFH).Methods: One hundred and twenty-five hFH subjects were studied. Plasma lipid, lipoprotein, vitamin B12, folic acid and Hcy values were determined. C677T polymorphism in the MTHFR gene was detected by SSCP-PCR. Genetic diagnosis of FH was determined by a three-step protocol using SSCP-PCR, Southern blot, long PCR and automatic sequencing.Results: We found significant differences in plasma HDL-C (CC 1.39±0.34, CT 1.33±0.39 and TT 1.14±0.26 mmol/L, p=0.028) between th…

AdultMalemedicine.medical_specialtyHeterozygoteApolipoprotein BHomocysteineHypercholesterolemiaFamilial hypercholesterolemiaPolymerase Chain Reactionchemistry.chemical_compoundInternal medicineGenotypeInternal MedicinemedicineHumansVitamin B12HomocysteineMethylenetetrahydrofolate Reductase (NADPH2)Polymorphism Single-Stranded ConformationalApolipoproteins BGeneticsPolymorphism GeneticbiologyCholesterolbusiness.industryBiochemistry (medical)Cholesterol HDLMiddle Agedmedicine.diseaseEndocrinologychemistryReceptors LDLMethylenetetrahydrofolate reductaseMutationbiology.proteinFemaleCardiology and Cardiovascular MedicinebusinessLipoproteinJournal of atherosclerosis and thrombosis
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Mutations in the skeletal muscle alpha-actin gene in patients with actin myopathy and nemaline myopathy

1999

Muscle contraction results from the force generated between the thin filament protein actin and the thick filament protein myosin, which causes the thick and thin muscle filaments to slide past each other. There are skeletal muscle, cardiac muscle, smooth muscle and non-muscle isoforms of both actin and myosin. Inherited diseases in humans have been associated with defects in cardiac actin (dilated cardiomyopathy and hypertrophic cardiomyopathy), cardiac myosin (hypertrophic cardiomyopathy) and non-muscle myosin (deafness). Here we report that mutations in the human skeletal muscle alpha-actin gene (ACTA1) are associated with two different muscle diseases, 'congenital myopathy with excess o…

AdultMalemedicine.medical_specialtyMyofilamentAdolescentDNA Mutational AnalysisMolecular Sequence Datamacromolecular substancesBiologyMyopathies NemalineTPM203 medical and health sciences0302 clinical medicineNemaline myopathyMuscular DiseasesInternal medicineMyosinGeneticsmedicineHumansPoint MutationAmino Acid SequenceChildMuscle SkeletalPolymorphism Single-Stranded ConformationalActin030304 developmental biologyFamily Health0303 health sciencesPolymorphism GeneticBase SequenceSequence Homology Amino AcidInfantSkeletal muscleDNASequence Analysis DNAmedicine.diseaseCongenital myopathyActins3. Good healthEndocrinologymedicine.anatomical_structureAmino Acid SubstitutionChild PreschoolMutationFemaleMYH7030217 neurology & neurosurgery
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