Search results for "Pedigree"

showing 10 items of 313 documents

Analysis of the RET, GDNF, EDN3, and EDNRB genes in patients with intestinal neuronal dysplasia and Hirschsprung disease

2001

BACKGROUNDHirschsprung disease (HSCR) is a frequent congenital disorder with an incidence of 1 in 5000 live births, characterised by the absence of parasympathetic intramural ganglion cells in the hindgut resulting in intestinal obstruction in neonates and severe constipation in infants and adults. Intestinal neuronal dysplasia (IND) shares clinical features with HSCR but the submucosal parasympathetic plexus is affected. IND has been proposed as one of the most frequent causes of chronic constipation and is often associated with HSCR.METHODSWe examined 29 patients diagnosed with sporadic HSCR, 20 patients with IND, and 12 patients with mixed HSCR/IND for mutations in the coding regions of …

Pathologymedicine.medical_specialtyGlial Cell Line-Derived Neurotrophic Factor ReceptorsHirschsprung diseaseMUTATION ANALYSISNerve Tissue ProteinsTYROSINE KINASEEDNRBArticleExonGermline mutationProto-Oncogene ProteinsNEUROTROPHIC FACTOR GDNFmedicineGlial cell line-derived neurotrophic factorDrosophila ProteinsHumansGlial Cell Line-Derived Neurotrophic FactorNerve Growth FactorsAlleleintestinal neuronal dysplasiaAllelesPolymorphism Single-Stranded ConformationalIntestinal neuronal dysplasiabiologyReceptors EndothelinSHAH-WAARDENBURG SYNDROMEProto-Oncogene Proteins c-retENDOTHELIN-B-RECEPTORMULTIGENIC INHERITANCEGastroenterologyReceptor Protein-Tyrosine KinasesSequence Analysis DNAGERMLINE MUTATIONSbiochemical phenomena metabolism and nutritionPROTOONCOGENEmedicine.diseasePHENOTYPIC-EXPRESSIONGDNFPedigreeProto-Oncogene Proteins c-retDysplasiaCase-Control StudiesMutationbiology.proteinLIGANDRETCongenital disorderEDN3
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Novel alpha-galactosidase A mutation in a female with recurrent strokes.

2012

Abstract Anderson–Fabry disease (AFD) is an X-linked inborn error of glycosphingolipid catabolism resulting from the deficient activity of the lysosomal exoglycohydrolase, a-galactosidase A. The complete genomic and cDNA sequences of the human alpha-galactosidase A gene have been determined and to date, several disease-causing alpha-galactosidase A mutations have been identified, including missense mutations, small deletions/insertions, splice mutations, and large gene rearrangements We report a case of a 56-year-old woman with recurrent cryptogenic strokes. Ophthalmological examination revealed whorled opacities of the cornea (cornea verticillata) and dilated tortuous conjunctival vessels.…

Pathologymedicine.medical_specialtyHeterozygoteClinical BiochemistryMolecular Sequence DataMutation MissenseBiologymedicine.disease_causeExonRecurrencemedicineMissense mutationHumansCornea verticillataAmino Acid SequenceGeneMutationBase SequencePoint mutationGeneral MedicineSequence Analysis DNAMiddle Agedmedicine.diseaseFabry diseaseMolecular biologyAngiokeratomaPedigreeStrokealpha-GalactosidaseFabry DiseaseFemalemedicine.symptomClinical biochemistry
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Autosomal recessive micrencephaly with simplified gyral pattern, abnormal myelination and arthrogryposis.

1999

The clinical courses, neuroimaging and muscle biopsy findings of two infants born to an inbred Arab family are described. They had a syndrome of micrencephaly with simplified gyral pattern, abnormal myelin formation and arthrogryposis. Increased variation of fiber size was seen in the muscle biopsy, creatine kinase, however was normal. Large areas of muscle were replaced by adipofibrous tissue. The infants had dysmorphic features consistent with the fetal akinesia/hypokinesia sequence. The abnormalities were suggestive of microlissencephaly probably associated with a dysgenetic process in the muscles. The syndrome showed an autosomal recessive inheritance.

Pathologymedicine.medical_specialtyMicrocephalyLissencephalyChromosome DisordersGenes RecessiveCentral nervous system diseaseConsanguinityHypokinesiaBiopsymedicineHumansMuscle SkeletalMyelin SheathArthrogryposisArthrogryposisChromosome AberrationsMuscle biopsymedicine.diagnostic_testbusiness.industryInfant NewbornBrainInfantGeneral MedicineAnatomySyndromemedicine.diseaseMagnetic Resonance ImagingMicrencephalyPedigreeSpinal CordPediatrics Perinatology and Child HealthMicrocephalyFemaleNeurology (clinical)medicine.symptombusinessFollow-Up StudiesNeuropediatrics
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Disease expression in women with hereditary angioedema

2008

Udgivelsesdato: 2008-Jun-11 OBJECTIVE: Fluctuations in sex hormones can trigger angioedema attacks in women with hereditary angioedema. Combined oral contraceptive therapies, as well as pregnancy, can induce severe attacks. The course of angioedema may be very variable in different women. STUDY DESIGN: Within the PREHAEAT project launched by the European Union, data on 150 postpubertal women with hereditary angioedema were collected in 8 countries, using a patient-based questionnaire. RESULTS: Puberty worsened the disease for 62%. Combined oral contraceptives worsened the disease for 79%, whereas progestogen-only pills improved it for 64%. During pregnancies, 38% of women had more attacks, …

PediatricsDiseaseMESH: HormonesMESH: Pregnancy0302 clinical medicinePregnancyMESH: ProgesteroneMESH: ChildImmunopathologyMESH: Contraceptives Oral CombinedMESH: Puberty030212 general & internal medicineskin and connective tissue diseasesProgesteronemedia_commonMESH: Middle AgedMESH: Complement Hemolytic Activity AssayMESH: Angioedema HereditaryVaginal deliveryfood and beveragesObstetrics and GynecologyMESH: Complement C4[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismMiddle AgedMenstruation3. Good healthContraceptives Oral CombinedMESH: Pregnancy ComplicationsPillHereditary angioedemaFemalemedicine.symptomAdultmedicine.medical_specialtyMESH: PedigreeMESH: Complement C1 Inactivator ProteinsMESH: Menstruation[SDV.MHEP.GEO]Life Sciences [q-bio]/Human health and pathology/Gynecology and obstetrics03 medical and health sciencesmedicineMESH: AngioedemaHumansmedia_common.cataloged_instanceEuropean unionPregnancyMESH: HumansAngioedemabusiness.industryPubertyAngioedemas HereditaryMESH: AdultDelivery Obstetricmedicine.diseaseHormonesMESH: RecurrenceSurgeryMESH: Abdominal PainPregnancy Complications030228 respiratory systemMESH: Delivery ObstetricbusinessMESH: FemaleAmerican Journal of Obstetrics and Gynecology
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Maternal phenylketonuria in two Sicilian families identified by maternal blood phenylalanine level screening and identification of a new phenylalanin…

1999

not available

Phenylketonuria MaternalPhenylalanine hydroxylasephenylalanine 4 monooxygenasePhenylalanineGene mutationMaternal bloodNeonatal ScreeningPregnancyPhenylketonuriasMedicineHumansMaternal phenylketonuriaGenetic TestingPhenylalanine levelGeneticsbiologybusiness.industryInfant NewbornPhenylalanine HydroxylasePedigreeItalyPediatrics Perinatology and Child HealthMutationbiology.proteinIdentification (biology)FemalebusinessEuropean journal of pediatrics
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Lecithin-cholesterol-acyltransferase deficiency: autosomal recessive transmission in a large kindred.

2008

Thirty-four members of a single Sardinian kindred with lecithin-cholesterol-acyltransferase deficiency have been studied. The kindred spans four generations and the parents of the two affected siblings are blood relatives. Segregation of the acyltransferase deficiency gene in the family clearly demonstrated an autosomal recessive mode of inheritance. Thirteen family members, including all obligate heterozygotes, had roughly half-normal acyltransferase activities (mean +/- S.D. = 0.39 +/- 0.06 mU/ml) when compared to 17 intrafamilial controls and spouses (mean +/- S.D. = 0.72 +/- 0.09 mU/ml) and 40 blood donors from Marburg/Lahn (mean +/- S.D. =0.76 +/- 0.1 mU/ml). Characterization of the he…

Plasma lipoproteinMaleHeterozygoteThalassemiaLipoproteinsGenes RecessiveConsanguinityConsanguinityLecithin Cholesterol Acyltransferase DeficiencyGeneticsmedicineHumansGenetics (clinical)GeneticsLecithin cholesterol acyltransferase deficiencybiologyHeterozygote advantagemedicine.diseaseHypolipoproteinemiasPedigreeAcyltransferaseLecithin—cholesterol acyltransferasebiology.proteinThalassemiaFemaleHypolipoproteinemiaClinical genetics
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The genetic structure of Norway

2020

AbstractThe aim of the present study was to describe the genetic structure of the Norwegian population using genotypes from 6369 unrelated individuals with detailed information about places of residence. Using standard single marker- and haplotype-based approaches, we report evidence of two regions with distinctive patterns of genetic variation, one in the far northeast, and another in the south of Norway, as indicated by fixation indices, haplotype sharing, homozygosity, and effective population size. We detect and quantify a component of Uralic Sami ancestry that is enriched in the North. On a finer scale, we find that rates of migration have been affected by topography like mountain ridg…

PopulationPopulationContext (language use)NorwegianArticleGene flowDanish03 medical and health sciencesEffective population sizeGenetic variationGeneticsHumansGenetic variationeducationGenetics (clinical)030304 developmental biology0303 health scienceseducation.field_of_studyPolymorphism GeneticNorwayEcology030305 genetics & hereditylanguage.human_languagePedigreeFixation (population genetics)GeographyHaplotypesGenetic structurelanguageGenetic markersVDP::Samfunnsvitenskap: 200
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Weyers acrodental dysostosis in a family.

1984

A four generation family with postaxial polydactyly of hands and feet and dental anomalies is reported. Lower and upper incisors were abnormal in shape and number. Additional findings were prominent ear anthelices, hypoplastic and dysplastic nails and mild shortness of stature. Inheritance was dominant with variable expression. It is proposed that the family presents the syndrome of acrofacial dysostosis described by Weyers in 1952. To differentiate it from other acrofacial dysostoses, we suggest naming the condition acrodental dysostosis.

Postaxial polydactylyMaleDental anomaliesNail dysplasiaWeyers acrodental dysostosisbusiness.industryTooth AbnormalitiesDysostosisAnatomyToesmedicine.diseaseDysostosesPedigreeVariable ExpressionFingersDysplastic nailsGeneticsmedicineHumansAbnormalities MultipleFemalebusinessChildGenetics (clinical)Clinical genetics
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Novel CREB3L3 Nonsense Mutation in a Family With Dominant Hypertriglyceridemia.

2015

Objective— Cyclic AMP responsive element–binding protein 3–like 3 ( CREB3L3 ) is a novel candidate gene for dominant hypertriglyceridemia. To date, only 4 kindred with dominant hypertriglyceridemia have been found to be carriers of 2 nonsense mutations in CREB3L3 gene (245fs and W46X). We investigated a family in which hypertriglyceridemia displayed an autosomal dominant pattern of inheritance. Approach and Results— The proband was a 49-year-old woman with high plasma triglycerides (≤1300 mg/dL; 14.68 mmol/L). Her father had a history of moderate hypertriglyceridemia, and her 51-year-old brother had triglycerides levels as high as 1600 mg/dL (18.06 mmol/L). To identify the causal mutation …

ProbandAdultMaleCandidate geneHeterozygoteSettore MED/09 - Medicina InternaHeredityAdolescentNonsense mutationDNA Mutational AnalysisPenetranceBiologymedicine.disease_causeSeverity of Illness IndexFrameshift mutationExonYoung AdultmedicineHumansGenetic Predisposition to DiseasetriglycerideCyclic AMP Response Element-Binding ProteinTriglyceridesAgedGeneticsAged 80 and overHypertriglyceridemiaMutationHypertriglyceridemiaMiddle Agedmedicine.diseasePenetrancePedigreePhenotypeCodon NonsenseFemalemutationCardiology and Cardiovascular MedicineBiomarkersArteriosclerosis, thrombosis, and vascular biology
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A family with various symptomatology suggestive of Anderson-Fabry disease and a genetic polymorphism of alpha galactosidase A gene.

2014

Background: Anderson/Fabry disease expresses a wide range of clinical variability in patients that it is possible to explain referring to a genetic variability with numerous mutations described in the literature (more than 600). Methods: We report some clinical cases of some members of a Sicilian family to express phenotypical variability of this disease in subjects with the same genetic mutation. Results: The first case was a 59-year-old female. Brain MRI revealed right frontal periventricular white matter of likely vascular-degenerative origin. The proband's alpha galactosidase A activity was 3.7. nmol/mL/h. Molecular genetics revealed a polymorphism: - 10 C. >. T; IVS 2-76_80del5; IVS…

ProbandAdultMalemedicine.medical_specialtyPathologySettore MED/09 - Medicina InternaAdolescentClinical BiochemistryMolecular Sequence DataBiologyAnderson-Fabry diseaseNucleic Acid DenaturationGastroenterologyPolymorphism (computer science)Internal medicineMolecular geneticsmedicineHaplotypeHumansFamilyGenetic Predisposition to DiseaseGenetic variabilitySymptomatologyChildPolymorphism GeneticBase SequenceHaplotypeHeterozygote advantageGeneral MedicineMiddle Agedmedicine.diseaseFabry diseaseMagnetic Resonance ImagingPedigreealpha-GalactosidaseFabry DiseaseMicroalbuminuriaFemaleHumanClinical biochemistry
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