Search results for " sequence"

showing 10 items of 3643 documents

Autonomic cardiac regulation in obstructive sleep apnea syndrome: evidence from spontaneous baroreflex analysis during sleep

1997

Objective. To assess spontaneous baroreceptor-heart rate reflex sensitivity during sleep in patients with obstructive sleep apnea syndrome, a condition associated with increased cardiovascular morbidity and mortality and characterized by marked sympathetic activation, which is believed to originate from hypoxic chemoreceptor stimulation, although little is known of other possible mechanisms such as baroreflex impairment. Design and methods. In 11 patients with severe obstructive sleep apnea syndrome (mean ± SD age 46.8 ± 8.1 years, apnea/hypopnea index 67.9 ± 19.1 h), who were normotensive or borderline hypertensive during wakefulness by clinic blood pressure measurements, finger blood pres…

AdultMalePhysiologyPolysomnographyBlood PressurePolysomnographySettore MED/10 - Malattie Dell'Apparato RespiratorioBaroreflexAutonomic Nervous SystemSleep Apnea SyndromesHeart RateHeart rateInternal MedicinemedicineHumansBaroreflex sensitivity Blood pressure Hypertension Obstructive sleep apnea Sequence technique Sympathetic nervous systemmedicine.diagnostic_testbusiness.industryApneaSleep apneaElectroencephalographyHeartBaroreflexBlood Pressure Monitoring AmbulatoryMiddle Agedmedicine.diseaseChemoreceptor CellChemoreceptor CellsObstructive sleep apneaBlood pressureAnesthesiaHypertensionFemalemedicine.symptomCardiology and Cardiovascular MedicinebusinessHypopneaHuman
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Detection of HIV type 1 non-B subtypes in Sicily, Italy.

2004

To evaluate the presence of HIV-1 non-B subtypes in Sicily, we sequenced and genotyped HIV-1 PR and RT regions of the pol gene using plasma from 169 HIV-1-infected adult patients. All samples were obtained from a study of antiretroviral-associated resistance mutations resulting in virological failure during highly active antiretroviral therapy (HAART). Eight (4.7%) patients had the non-B HIV-1 subtype including some circulating recombinant forms (CRFs). All of these individuals acquired the infection by heterosexual transmission. The detection of HIV-1 non-B strains was significantly associated with younger age of HIV-1 acquisition. Our findings indicate, for the first time, the presence of…

AdultMalePol genesYounger ageImmunologyMolecular Sequence DataHuman immunodeficiency virus (HIV)HIV Infectionsmedicine.disease_causeVirusVirologyAntiretroviral Therapy Highly ActiveDrug Resistance ViralmedicineHumansIn patientTreatment FailurebiologyAdult patientsvirus diseasesMiddle Agedbiology.organism_classificationAntiretroviral therapyVirologyGenes polInfectious DiseasesItalyLentivirusImmunologyMutationHIV-1RNA ViralFemaleAIDS research and human retroviruses
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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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Muscular synergies during motor corrections: investigation of the latencies of muscle activities.

2010

To reduce the complexity of muscular control, a small number of muscular activations are combined to produce an infinity of movements. This concept of muscle synergies has been widely investigated, mainly by means of principal component analyses (PCA) in the case of unperturbed movements. However, reaching movements can be altered at any time if the target location is changed during their execution. In this case, PCA does not precisely measure the latencies of muscles activities. We develop here a simple method to investigate how a random target jump toward a single location induced motor corrections in the whole musculature by precisely determining the latencies of muscle activities during…

AdultMalePrincipal Component AnalysisTime Factorsmedicine.diagnostic_testMotor sequenceMovement (music)Computer scienceElectromyographyMovementMotor controlElectromyographyHandFunctional systemBiomechanical PhenomenaBehavioral NeuroscienceElectrophysiologymedicineJumpReaction TimeHumansLatency (engineering)Muscle SkeletalNeuroscienceBehavioural brain research
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Autosomal recessive hypercholesterolemia in a Sicilian kindred harboring the 432insA mutation of the ARH gene

2003

Abstract We describe a Sicilian family presenting a recessive form of hypercholesterolemia harboring a mutation of the autosomal recessive hypercholesterolemia (ARH) gene. In two of the three sibs, a 26-year-old male and a 22-year-old female, a severe hypercholesterolemia was diagnosed with very high levels of plasma cholesterol (15.9 and 12.2 mmol/l, respectively); tendon xanthomatas and xanthelasms were present and in the male proband was documented a diffuse coronary atherosclerotic disease with a rapid and fatal progression. Both the parents had normal or slightly increased levels of plasma cholesterol. All causes of secondary hypercholesterolemia were ruled out as well as an involvemen…

AdultMaleProbandHeterozygotemedicine.medical_specialtyApolipoprotein BDNA Mutational AnalysisMolecular Sequence DataGenes RecessiveARH geneCoronary AngiographyRisk AssessmentGenetic determinismHyperlipoproteinemia Type IIInternal medicinemedicineHumansPoint MutationRNA MessengerSicilyGeneAdaptor Proteins Signal TransducingHypolipidemic AgentsGeneticsBase SequencebiologySiblingsCoronary StenosisHeterozygote advantageAutosomal recessive hypercholesterolemiaPedigreeAdaptor Proteins Vesicular TransportTreatment OutcomeEndocrinologyAutosomal Recessive HypercholesterolemiaMutationLDL receptorMutation (genetic algorithm)biology.proteinFemalelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineFollow-Up StudiesAtherosclerosis
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Novel LMF1 nonsense mutation in a patient with severe hypertriglyceridemia

2009

Context: Lipase maturation factor 1 (LMF1) gene is a novel candidate gene in severe hypertriglyceridemia. Lmf1 is involved in the maturation of lipoprotein lipase (LPL) and hepatic lipase in endoplasmic reticulum. To date only one patient with severe hypertriglyceridemia and related disorders was found to be homozygous for a nonsense mutation in LMF1 gene (Y439X).Objective: The objective of the study was to investigate LMF1 gene in hypertriglyceridemic patients in whom mutations in LPL, APOC2, and APOA5 genes had been excluded.Results: The resequencing of LMF1 gene led to the discovery of a novel homozygous nonsense mutation in one patient with severe hypertriglyceridemia and recurrent epis…

AdultMaleProbandmedicine.medical_specialtyCandidate geneEndocrinology Diabetes and MetabolismMolecular Sequence DataClinical BiochemistryNonsense mutationContext (language use)macromolecular substances030204 cardiovascular system & hematologyBiologyBiochemistry03 medical and health sciencesExon0302 clinical medicineEndocrinologyInternal medicinemedicineHumansTriglyceridesHypolipidemic Agents030304 developmental biologyHypertriglyceridemia0303 health sciencesLipoprotein lipaseBase Sequencedigestive oral and skin physiologyBiochemistry (medical)Hypertriglyceridemianutritional and metabolic diseasesGenetic VariationLMF1 gene; nonsense mutation; hypertriglyceridemiaLMF1 hypertriglyceridemiamedicine.disease3. Good healthLipoprotein LipaseEndocrinologyCodon NonsenseOriginal Articlelipids (amino acids peptides and proteins)Hepatic lipaseGemfibrozil
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De novo mutation in a male patient with Fabry disease: a case report

2014

Abstract Background Fabry disease is an X-linked inherited metabolic condition where the deficit of the α-galactosidase A enzyme, encoded by the GLA gene, leads to glycosphingolipid storage, mainly globotriaosylceramide. To date, more than 600 mutations have been identified in human GLA gene that are responsible for FD, including missense and nonsense mutations, small and large deletions. Such mutations are usually inherited, and cases of de novo onset occur rarely. Case presentation In this article we report an interesting case of a 44-year-old male patient suffering from a severe form of Fabry disease, with negative family history. The patient showed signs such as cornea verticillata, ang…

AdultMaleProtein Foldingα-galactosidase ADe novo mutationNonsense mutationD165H mutationGlobotriaosylceramideMutation MissenseCase ReportBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundGermline mutationmedicineMissense mutationHumansPoint MutationThrombophiliaEnzyme Replacement TherapyAmino Acid SequenceChildGLA geneConserved SequenceGerm-Line MutationMedicine(all)GeneticsMutationFabry diseaseSequence Homology Amino AcidBiochemistry Genetics and Molecular Biology(all)Point mutationGeneral MedicineEnzyme replacement therapymedicine.diseaseFabry diseasePedigreeStrokechemistryAmino Acid Substitutionalpha-GalactosidaseKidney Failure ChronicFemaleSymptom AssessmentSequence AlignmentBMC Research Notes
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Local administration of antisense phosphorothioate oligonucleotides to the p65 subunit of NF-kappa B abrogates established experimental colitis in mi…

1996

Chronic intestinal inflammation induced by 2,4,6,-trinitrobenzene sulfonic acid (TNBS) is characterized by a transmural granulomatous colitis that mimics some characteristics of human Crohn's disease. Here, we show that the transcription factor NF-kappa B p65 was strongly activated in TNBS-induced colitis and in colitis of interleukin-10-deficient mice. Local administration of p65 antisense phosphorothioate oligonucleotides abrogated clinical and histological signs of colitis and was more effective in treating TNBS-induced colitis than single or daily administration of glucocorticoids. The data provide direct evidence for the central importance of p65 in chronic intestinal inflammation and …

AdultMaleProtein subunitMolecular Sequence DataGeneral Biochemistry Genetics and Molecular BiologyMiceCrohn DiseaseAdrenal Cortex HormonesmedicineAnimalsHumansColitisTranscription factorCells CulturedAgedEnterocolitisPhosphorothioate OligonucleotidesBase Sequencebusiness.industryOligonucleotideEnterocolitisNF-kappa BTranscription Factor RelAGeneral MedicineDNAMiddle AgedOligonucleotides Antisensemedicine.diseaseNFKB1digestive system diseasesInterleukin-10Interleukin 10Disease Models AnimalTrinitrobenzenesulfonic AcidImmunologyCancer researchCytokinesFemalemedicine.symptombusinessNature medicine
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Mutations in ARL2BP, Encoding ADP-Ribosylation-Factor-Like 2 Binding Protein, Cause Autosomal-Recessive Retinitis Pigmentosa

2013

Retinitis pigmentosa (RP) is a genetically heterogeneous retinal degeneration characterized by photoreceptor death, which results in visual failure. Here, we used a combination of homozygosity mapping and exome sequencing to identify mutations in ARL2BP, which encodes an effector protein of the small GTPases ARL2 and ARL3, as causative for autosomal-recessive RP (RP66). In a family affected by RP and situs inversus, a homozygous, splice-acceptor mutation, c.101−1G>C, which alters pre-mRNA splicing of ARLBP2 in blood RNA, was identified. In another family, a homozygous c.134T>G (p.Met45Arg) mutation was identified. In the mouse retina, ARL2BP localized to the basal body and cilium-associated…

AdultMaleRetinal degenerationCentrioleMolecular Sequence DataGenes RecessiveBiologymedicine.disease_causeMice03 medical and health sciences0302 clinical medicineBardet–Biedl syndromeGTP-Binding ProteinsReportRetinitis pigmentosaGeneticsmedicineAnimalsHumansBasal bodyGenetics(clinical)Photoreceptor CellsGenetics (clinical)030304 developmental biologyPrimary ciliary dyskinesiaGenetics0303 health sciencesMutationBase SequenceADP-Ribosylation FactorsCiliumHomozygoteMembrane Transport ProteinsEpithelial Cellsmedicine.diseasePedigreeCell biologyMutationFemalesense organsCarrier ProteinsRetinitis Pigmentosa030217 neurology & neurosurgeryProtein BindingTranscription FactorsThe American Journal of Human Genetics
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Gly114Asp mutation of rhodopsin in autosomal dominant retinitis pigmentosa

1995

Two autosomal dominant retinitis pigmentosa families of different origin were screened for rhodopsin mutations using the method of single strand conformation polymorphism and direct sequencing. We found a CGG-CAG substitution in codon 114 of rhodopsin in both families. This change predicted the replacement of a glycine by an aspartic acid and suggested that this change is the cause of the disease in these families.

AdultMaleRhodopsincongenital hereditary and neonatal diseases and abnormalitiesAdolescentgenetic structuresMolecular Sequence DataGlycinemedicine.disease_causeAutosomal dominant retinitis pigmentosaRetinitis pigmentosaAspartic acidmedicineHumansPoint MutationAmino Acid SequenceCodonMolecular BiologyGenes DominantGeneticsAspartic AcidMutationPolymorphism GeneticBase SequencebiologyDirect sequencingSingle-strand conformation polymorphismCell BiologyMiddle Agedmedicine.diseasePedigreeRhodopsinGlycinebiology.proteinFemalesense organsRetinitis PigmentosaMolecular and Cellular Probes
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