Search results for "MUTATION"

showing 10 items of 2830 documents

Correlation between FIX genotype and pharmacokinetics of Nonacog alpha according to a multicentre Italian study

2016

Introduction Pharmacokinetic (PK) studies on recombinant FIX concentrate, Nonacog alpha, were conducted with different sampling time designs which gave rise to not complete and homogenous outcomes. In addition, patient's FIX genotype/PK relationship has never been investigated. Aim Investigate how different sampling times may affect PK parameters and try to find a FIX genotype/PK relationship. Patients and Methods A cohort pharmacokinetic, Nonacog Alpha single-dose, open-label, non-comparative study was conducted in eight Comprehensive Care Haemophilia Centres in Italy. Seventeen previously treated moderate or severe haemophilia B patients were enrolled. Factors IX:C one-stage clotting assa…

Malemedicine.medical_specialtyGenotypeMutation MissensePharmacokinetic030204 cardiovascular system & hematologyPharmacologyHaemophiliaGastroenterologyHemophilia BDrug Administration ScheduleCohort StudiesFactor IX03 medical and health sciences0302 clinical medicinePharmacokineticsDNA Recombinant proteinInternal medicineHaemophilia BGenotypemedicineHumansHaemophilia BGenetics (clinical)Volume of distributionClotting factorbusiness.industryCoagulantsArea under the curveGeneral MedicineHematologymedicine.diseaseRecombinant ProteinsItalyROC CurveCodon NonsenseArea Under Curvebusinesspharmacokinetics030215 immunologyBlood samplingHalf-Life
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Late-onset myasthenia gravis - CTLA4(low) genotype association and low-for-age thymic output of naïve T cells.

2014

Abstract Late-onset myasthenia gravis (LOMG) has become the largest MG subgroup, but the underlying pathogenetic mechanisms remain mysterious. Among the few etiological clues are the almost unique serologic parallels between LOMG and thymoma-associated MG (TAMG), notably autoantibodies against acetylcholine receptors, titin, ryanodine receptor, type I interferons or IL-12. This is why we checked LOMG patients for two further peculiar features of TAMG – its associations with the CTLA4 high/gain-of-function  +49A/A genotype and with increased thymic export of naive T cells into the blood, possibly after defective negative selection in AIRE-deficient thymomas. We analyzed genomic DNA from 116 …

Malemedicine.medical_specialtyGenotypeThymomaT-LymphocytesImmunologyDNA Mutational AnalysisRecent Thymic EmigrantLate onsetCell CountThymus GlandBiologyPeripheral blood mononuclear cellWhite PeopleGene FrequencyInternal medicineGenotypeMyasthenia GravismedicineImmune ToleranceImmunology and AllergyHumansCTLA-4 AntigenGenetic Predisposition to DiseaseGenetic Association StudiesAgedPeripheral tolerance inductionAged 80 and overPolymorphism GeneticThymocytesT-cell receptor excision circlesAutoantibodyCell DifferentiationThymus NeoplasmsMiddle Agedmedicine.diseaseMyasthenia gravisEndocrinologyImmunologyFemaleJournal of autoimmunity
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ITPA deficiency and ribavirin level are still predictive of anaemia in HCV–HIV-coinfected patients receiving ribavirin combined with a first-generati…

2017

Background We aimed to determine the impact of inosine triphosphatase (ITPA) deficiency on ribavirin (RBV)-induced anaemia in HIV–HCV-coinfected patients receiving a triple therapy including the haematotoxic direct-acting antiviral agent boceprevir (BOC). Methods Patients of the ANRS HC27 BocepreVIH study were genotyped for two ITPA single nucleotide polymorphisms involved in ITPA deficiency. RBV trough concentration (Ctrough) was determined at week (W)4 and W8. Impact of ITPA deficiency on anaemia, RBV Ctrough, response and haematotoxicity (grade 3/4 anaemia, erythropoietin [EPO] use, RBV dose reduction or transfusion between day [D]0 and W8) was evaluated. Impact of RBV Ctrough on anaemia…

Malemedicine.medical_specialtyGenotype[SDV]Life Sciences [q-bio]Human immunodeficiency virus (HIV)HIV Infectionsmedicine.disease_causeAntiviral AgentsGastroenterologychemistry.chemical_compoundPharmacotherapyGene FrequencyRisk FactorsInternal medicineRibavirinmedicineHumansGenetic Predisposition to DiseasePharmacology (medical)PyrophosphatasesAllelesComputingMilieux_MISCELLANEOUSPharmacologyCoinfectionbusiness.industryRibavirinAnemiaHepatitis CHepatitis C ChronicMiddle Agedmedicine.diseaseFirst generation3. Good health[SDV] Life Sciences [q-bio]Infectious DiseaseschemistryMutationCoinfectionDrug Therapy CombinationFemaleITPAbusinessMetabolism Inborn ErrorsINOSINE TRIPHOSPHATASE
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Polymorphism in the peroxisome proliferator-activated receptor ? gene influences the risk for Alzheimer?s disease

2003

The peroxisome proliferator-activated receptor alpha (PPAR-alpha) is a member of the steroid hormone super family of ligand-inducible transcription factors, involved in glucose and lipid metabolism. We screened for polymorphisms in the PPAR-alpha gene and detected two known polymorphisms located in exon 5 and intron 7. These polymorphisms were investigated for their possible association with Alzheimer's disease (AD) and for their effect in carriers of an insulin gene (INS) polymorphism. The PPAR-alpha C --G polymorphism in exon 5 (L162V) was associated with AD, in that the V-allele was more frequent in AD patients than in healthy subjects. Further data analysis revealed that carriers of an …

Malemedicine.medical_specialtyGenotypemedicine.medical_treatmentDNA Mutational AnalysisReceptors Cytoplasmic and NuclearBiologyExonGene FrequencyAlzheimer DiseaseInternal medicineGenotypemedicineHumansInsulinGenetic Predisposition to DiseaseGenetic TestingAlleleReceptorAllele frequencyBiological PsychiatryAgedAged 80 and overAmyloid beta-PeptidesPolymorphism GeneticExonsMiddle Agedmedicine.diseasePsychiatry and Mental healthSteroid hormoneEndocrinologyAmino Acid SubstitutionNeurologyFemaleNeurology (clinical)Peroxisome proliferator-activated receptor alphaAlzheimer's diseaseTranscription FactorsJournal of Neural Transmission
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A new heterozygous mutation (L338N) in the human Gsalpha (GNAS1) gene as a cause for congenital hypothyroidism in Albright's hereditary osteodystroph…

2003

OBJECTIVE: To identify the molecular defect by which psychomotor retardation is caused in two brothers with congenital hypothyroidism who received adequate treatment with l-thyroxine. CASE REPORT: A six-year-old boy presented with psychomotor retardation and congenital primary hypothyroidism (CH). The patient had a normal blood thyrotrophin (TSH) level on neonatal screening, but low total serum thyroxine and triiodothyronine concentrations prompting thyroid hormone substitution shortly after birth. Nevertheless, psychomotor development was retarded and the patient underwent further investigation. Typical features of Albright's hereditary osteodystrophy (AHO) such as round face, obesity, and…

Malemedicine.medical_specialtyHeterozygoteGenotypeEndocrinology Diabetes and MetabolismThyrotropinFibrous Dysplasia PolyostoticEndocrinologyHypothyroidismInternal medicinemedicineGTP-Binding Protein alpha Subunits GsHumansOsteodystrophyChildAlbright's hereditary osteodystrophyPseudohypoparathyroidismPsychomotor retardationbusiness.industryThyroidErythrocyte MembranePrimary hypothyroidismGeneral MedicineSequence Analysis DNAmedicine.diseaseCongenital hypothyroidismPedigreeThyroxineEndocrinologymedicine.anatomical_structureMutationTriiodothyroninePseudopseudohypoparathyroidismCalciummedicine.symptomMetacarpusPsychomotor DisordersbusinessEuropean journal of endocrinology
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Prenatal diagnosis and carrier detection in mucopolysaccharidosis type II by mutation analysis. A 47,XXY male heterozygous for a missense point mutat…

1994

Identification of iduronate-2-sulphatase (IDS) gene mutations in patients with mucopolysaccharidosis type II (MPS II, Hunter syndrome) allows fast and reliable carrier detection and prenatal diagnosis. We describe here three cases of prenatal diagnosis by direct detection of the gene mutation. In addition to two affected male fetuses from two different families, a 47,XXY fetus carrying both the normal and the mutant allele was diagnosed in a third family. The latter pregnancy was carried to term and the child is obviously not affected by MPS II.

Malemedicine.medical_specialtyHeterozygoteX ChromosomeMucopolysaccharidosisDNA Mutational AnalysisPrenatal diagnosisIduronate SulfataseGene mutationBiologyPregnancyInternal medicinePrenatal DiagnosismedicineMissense mutationHumansPoint MutationMucopolysaccharidosis type IIGenetics (clinical)AllelesSex Chromosome AberrationsMucopolysaccharidosis IIGeneticsPoint mutationGenetic Carrier ScreeningObstetrics and GynecologyHunter syndromeDNAmedicine.diseaseFetal DiseasesEndocrinologyKaryotypingFemaleKlinefelter syndromePrenatal diagnosis
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Hereditary Angioedema with Normal C1 Inhibitor

2013

Until recently it was assumed that hereditary angioedema was a disease that results exclusively from a genetic deficiency of the C1 inhibitor. In 2000, families with hereditary angioedema, normal C1 inhibitor activity, and protein in plasma were described. Since then, numerous patients and families with that condition have been reported. Most of the patients were women. In many of the affected women, oral contraceptives, hormone replacement therapy containing estrogens, and pregnancies triggered the clinical symptoms. In some families mutations in the coagulation factor XII (Hageman factor) gene were detected.

Malemedicine.medical_specialtyImmunologyCoagulation Factor XIIC1-inhibitorDiagnosis DifferentialPregnancyRisk FactorsInternal medicinemedicineHumansImmunology and AllergyHereditary Angioedema Type IIIAngioedemaFactor XIIbiologyAngioedemabusiness.industryAngioedemas Hereditarymedicine.diseaseEndocrinologyTransgender hormone therapyFactor XIIMutationHereditary angioedemabiology.proteinFemaleDifferential diagnosismedicine.symptombusinessComplement C1 Inhibitor ProteinImmunology and Allergy Clinics of North America
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Structural dissimilarities in different regions of the pineal gland of Pirbright white guinea-pigs.

1982

In the present study, the proximal, intermediate and distal parts of dumbbell-shaped pineal glands of Pirbright White guinea-pigs were investigated with respect to structural dissimilarities. The most conspicuous difference was that while in the proximal part the pinealocytes were arranged in a random fashion, the intermediate and distal regions, except a small ventral area in the latter, exhibited a prominent follicular arrangement of the pinealocytes. Concretions were restricted to the subcapsular region of the intermediate part, whereas cells with hyperchromatic nuclei increased in number in an anterior-posterior direction. In males, pinealocyte nuclear size did not differ significantly …

Malemedicine.medical_specialtyLightKaryometryGuinea PigsBiologyPineal GlandHyperchromatic nucleiPinealocytePineal glandSpecies SpecificityInternal medicineFollicular phasemedicineAnimalsHumansBiological PsychiatryNeuronsGenetic VariationHistologyAnatomyWhite (mutation)Psychiatry and Mental healthEndocrinologymedicine.anatomical_structureNeurologyFemaleNeurology (clinical)Journal of neural transmission
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Genetic deficiency of tartrate-resistant acid phosphatase associated with skeletal dysplasia, cerebral calcifications and autoimmunity

2010

Vertebral and metaphyseal dysplasia, spasticity with cerebral calcifications, and strong predisposition to autoimmune diseases are the hallmarks of the genetic disorder spondyloenchondrodysplasia. We mapped a locus in five consanguineous families to chromosome 19p13 and identified mutations in ACP5, which encodes tartrate-resistant phosphatase (TRAP), in 14 affected individuals and showed that these mutations abolish enzyme function in the serum and cells of affected individuals. Phosphorylated osteopontin, a protein involved in bone reabsorption and in immune regulation, accumulates in serum, urine and cells cultured from TRAP-deficient individuals. Case-derived dendritic cells exhibit an …

Malemedicine.medical_specialtyLymphocyteT cellAcid PhosphatasePhosphataseAutoimmunityOsteochondrodysplasiasmedicine.disease_causeBone and BonesAutoimmune DiseasesAutoimmunity03 medical and health sciences0302 clinical medicineInternal medicineGeneticsmedicineHumansGenetic Predisposition to DiseaseOsteopontinPhosphorylationChild030304 developmental biologyTartrate-resistant acid phosphatase030203 arthritis & rheumatologyBone Diseases Developmental0303 health sciencesbiologyTartrate-Resistant Acid PhosphataseHomozygoteBrainMetaphyseal dysplasiamedicine.disease3. Good healthIsoenzymesRadiographymedicine.anatomical_structureEndocrinologyDysplasiaMutationbiology.proteinCalciumOsteopontinNature Genetics
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The Clinical and Molecular Spectrum of GM1 Gangliosidosis

2019

Objective To evaluate the clinical presentation of patients with GM1 gangliosidosis and to determine whether specific clinical or biochemical signs could lead to a prompt diagnosis. Study design We retrospectively analyzed clinical, biochemical, and genetic data of 22 patients with GM1 gangliosidosis from 5 metabolic centers in Germany and Austria. Results Eight patients were classified as infantile, 11 as late-infantile, and 3 as juvenile form. Delay of diagnosis was 6 ± 2.6 months in the infantile, 2.6 ± 3.79 years in the late-infantile, and 14 ± 3.48 years in the juvenile form. Coarse facial features, cherry red spots, and visceromegaly occurred only in patients with the infantile form. …

Malemedicine.medical_specialtyMovement disordersAdolescentGenotypeUrinary systemDNA Mutational AnalysisDiseaseGastroenterologyYoung Adult03 medical and health sciences0302 clinical medicineGermany030225 pediatricsInternal medicineGenotypemedicineHumans030212 general & internal medicineChildRetrospective StudiesDystoniaGangliosidosis GM1Coarse facial featuresbusiness.industryIncidenceInfantDNAbeta-Galactosidasemedicine.diseaseDysphagiaPhenotypeAustriaChild PreschoolMutationPediatrics Perinatology and Child HealthATP-Binding Cassette TransportersFemalemedicine.symptombusinessVisceromegalyFollow-Up StudiesThe Journal of Pediatrics
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