Search results for "Pedigree"

showing 10 items of 313 documents

Hereditary angioedema with normal C1-inhibitor activity in women.

2000

Summary Background Hereditary angioedema (HAE) is a well defined autosomal dominant disease (Mendelian Inheritance in Man #106100) that results from an inherited deficiency of C1 (the activated first component of complement) inhibitor function. We report an unusual variant of HAE with normal biochemical C1-inhibitor function, occurring only in women. Methods We screened 574 patients with recurrent angioedema of the skin for presence of HAE. 283 patients were selected, in whom angioedema was associated with abdominal pain attacks or recurrent life-threatening episodes of upper-airway obstruction, or both, rather than with urticaria. We measured C1-inhibitor concentration and functional activ…

AdultMaleX ChromosomeAdolescentGenetic LinkageComplement C1 Inactivator ProteinsC1-inhibitorEcallantideSex FactorsRecurrenceTerminology as TopicmedicineHumansHereditary Angioedema Type IIISex RatioFamily historyAngioedemaChildDominance (genetics)Genes DominantAngioedemabiologybusiness.industryAutosomal dominant traitComplement C4General MedicineMiddle Agedmedicine.diseaseAbdominal PainPedigreeAirway ObstructionImmunologyHereditary angioedemaMutationbiology.proteinFemalemedicine.symptombusinessmedicine.drugLancet (London, England)
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Genotypic and phenotypic spectrum in tricho-rhino-phalangeal syndrome types I and III

2000

Tricho-rhino-phalangeal syndrome (TRPS) is characterized by craniofacial and skeletal abnormalities. Three subtypes have been described: TRPS I, caused by mutations in the TRPS1 gene on chromosome 8; TRPS II, a microdeletion syndrome affecting the TRPS1 and EXT1 genes; and TRPS III, a form with severe brachydactyly, due to short metacarpals, and severe short stature, but without exostoses. To investigate whether TRPS III is caused by TRPS1 mutations and to establish a genotype-phenotype correlation in TRPS, we performed extensive mutation analysis and evaluated the height and degree of brachydactyly in patients with TRPS I or TRPS III. We found 35 different mutations in 44 of 51 unrelated p…

AdultMaleanimal structuresAdolescentGenotypeDNA Mutational AnalysisMolecular Sequence DataLimb Deformities CongenitalBiologyOsteochondrodysplasiasPolymorphism Single NucleotideShort statureLanger–Giedion syndromeGeneticsmedicineHumansMissense mutationTricho–rhino–phalangeal syndromeGenetics(clinical)Amino Acid SequenceChildGenetics (clinical)GeneticsAnthropometryBase SequenceBrachydactylyInfantZinc FingersExonsSyndromeArticlesMiddle AgedMicrodeletion syndromemedicine.diseasePenetranceBody HeightPedigreeDNA-Binding ProteinsRadiographyPhenotypeChild PreschoolMutationTrichorhinophalangeal Syndrome Type IErythroid-Specific DNA-Binding FactorsFemalemedicine.symptomChromosomes Human Pair 8Transcription Factors
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MFAP5 Loss-of-Function Mutations Underscore the Involvement of Matrix Alteration in the Pathogenesis of Familial Thoracic Aortic Aneurysms and Dissec…

2014

Thoracic aortic aneurysm and dissection (TAAD) is an autosomal-dominant disorder with major life-threatening complications. The disease displays great genetic heterogeneity with some forms allelic to Marfan and Loeys-Dietz syndrome, and an important number of cases still remain unexplained at the molecular level. Through whole-exome sequencing of affected members in a large TAAD-affected family, we identified the c.472CT (p.Arg158(∗)) nonsense mutation in MFAP5 encoding the extracellular matrix component MAGP-2. This protein interacts with elastin fibers and the microfibrillar network. Mutation screening of 403 additional probands identified an additional missense mutation of MFAP5 (c.62GT …

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesAdolescentExtracellular matrix componentNonsense mutationHaploinsufficiencyThoracic aortic aneurysmPathogenesisContractile ProteinsReportGeneticsmedicineHumansMissense mutationGenetics(clinical)ExomeChildGenetics (clinical)AgedGlycoproteinsAged 80 and overGeneticsAortic Aneurysm ThoracicbiologyGenetic heterogeneitySequence Analysis DNAFibroblastsMiddle Agedmedicine.diseasePedigree3. Good healthAortic DissectionAmino Acid SubstitutionCodon Nonsensebiology.proteinIntercellular Signaling Peptides and ProteinsFemaleHaploinsufficiencyElastinThe American Journal of Human Genetics
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Point mutations associated with Leber hereditary optic neuropathy in a Latvian population

2013

Purpose To study mutations associated with Leber hereditary optic neuropathy (LHON) in patients suspected of having this mitochondrial disorder in a Latvian population. Additional aims were to determine the heteroplasmy status of all non-synonymous polymorphisms identified in the current study and to identify the mitochondrial haplogroups of the studied participants because these factors may contribute to the manifestation of LHON. Methods Twelve patients, including patients in two families, were enrolled in the current study. LHON was suspected based on the findings of ophthalmologic examinations. In clinically affected individuals, the presence of all previously reported LHON-associated m…

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesPolymorphism Geneticgenetic structuresnutritional and metabolic diseasesOptic Atrophy Hereditary LeberSequence Analysis DNAMiddle AgedDNA MitochondrialLatviaeye diseasesWhite PeopleMitochondriaPedigreeHaplotypesHumansPoint MutationFemaleResearch Article
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One

2019

Neurofibromatosis type 1 (NF1) is an autosomal dominant disease with complete penetrance but high variable expressivity. NF1 is caused by loss-of-function mutations in the NF1 gene, a negative regulator of the RAS-MAPK pathway. The NF1 gene has one of the highest mutation rates in human disorders, which may explain the outbreak of independent de novo variants in the same family. Here, we report the co-occurrence of pathogenic variants in the NF1 and SPRED1 genes in six families with NF1 and Legius syndrome, using next-generation sequencing. In five of these families, we observed the co-occurrence of two independent NF1 variants. All NF1 variants were classified as pathogenic, according to t…

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesSPRED1Neurofibromatosis 1Neurofibromin 1AdolescentCafe-au-Lait Spotsneurofibromatosis type 1eye diseasesArticlenervous system diseasesPedigreeLegius syndromePhenotypeNF1MutationHumansFemalede novo variantChildneoplasmsAdaptor Proteins Signal TransducingGenes
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Subclinical hyperthyroidism due to a thyrotropin receptor (TSHR) gene mutation (S505R).

2006

Aim: To identify the molecular defect by which non-autoimmune subclinical hyperthyroidism was caused in a 6-mo-old infant who presented with weight loss. Methods: Congenital non-autoimmune hyperthyroidism is caused by activating germline mutations in the thyrotropin receptor (TSHR) gene. Therefore, the TSHR gene was sequenced directly from the patient's genomic DNA. Results: Molecular analysis revealed a heterozygous point mutation (S505R) in the TSHR gene as the underlying defect. Conclusion: A constitutively activating mutation in the TSHR gene has to be considered not only in patients with severe congenital non-autoimmune hyperthyroidism, but also in children with subclinical non-autoimm…

AdultMaleendocrine systemmedicine.medical_specialtyendocrine system diseasesAsymptomaticHyperthyroidismThyrotropin receptorTSHR Gene MutationGermline mutationInternal medicineMedicineMissense mutationHumansPoint MutationGeneSubclinical infectionbusiness.industryPoint mutationInfantReceptors ThyrotropinGeneral Medicineeye diseasesPedigreeEndocrinologyPediatrics Perinatology and Child HealthCancer researchFemalemedicine.symptombusinesshormones hormone substitutes and hormone antagonistsActa paediatrica (Oslo, Norway : 1992)
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God, Faith, and Death: The Impact of Biological and Religious Correlates on Mortality

2004

Marked denominational mortality differentials have been documented for various time periods and geographic locations. From a historical perspective, death rates among Catholics are often found to be higher than those among Protestants or Jews. Using a conceptual model based on the life history approach, biomedical and sociocultural factors of causation are extrapolated. In total, 5513 historical entries from family reconstitution were available. Selection of data was guided by the inclusion of information about religious affiliation. Only married couples with children as well as single mothers were considered. Of these, 1855 entries were of Roman Catholic (C), 1143 of Lutheran/Protestant (L…

AdultMalemedia_common.quotation_subjectLongevityReligiosityFaithSex FactorsProtestantismPregnancyRisk FactorsGermanyInfant MortalityGeneticsHumansSociologyMortalityCausationChildSociocultural evolutionGenetics (clinical)Ecology Evolution Behavior and Systematicsmedia_commonMortality rateCatholicismInfant NewbornPregnancy OutcomeHistorical demographySingle mothersSurvival AnalysishumanitiesPedigreeParityMaternal MortalityProtestantismSocioeconomic FactorsFemaleDemographyHuman Biology
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Hereditary angioedema with normal C1 inhibitor: clinical symptoms and course.

2007

Abstract Purpose A new type of hereditary angioedema was described recently. It was characterized by recurrent bouts of angioedema in various organs and normal C1 inhibitor and was observed mainly in women. Our aim was to conduct a detailed study of the clinical features of this condition. Methods A total of 138 patients with hereditary angioedema and normal C1 inhibitor who belonged to 43 unrelated families were examined through the use of standardized questionnaires. Results A majority of patients with hereditary angioedema and normal C1 inhibitor had skin swellings (92.8%), tongue swellings (53.6%), and abdominal pain attacks (50%). Laryngeal edema (25.4%) and uvular edema (21.7%) also w…

AdultMalemedicine.medical_specialtyAbdominal painPathologyComplement C1 Inactivator ProteinsLaryngeal EdemaC1-inhibitorTongueimmune system diseasesEdemamedicineHumansHereditary Angioedema Type IIIcardiovascular diseasesAngioedemaskin and connective tissue diseasesSerpinsAgedRetrospective StudiesSkinSex CharacteristicsErythema marginatumAngioedemabiologybusiness.industryfood and beveragesGeneral MedicineMiddle Agedmedicine.diseaseDermatologyPedigreeUvulaHereditary angioedemabiology.proteinFemalemedicine.symptombusinessComplement C1 Inhibitor ProteinThe American journal of medicine
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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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Increased sensitivity of the neuronal nicotinic receptor alpha-2 subunit causes familial epilepsy with nocturnal wandering and ictal fear

2006

Sleep has traditionally been recognized as a precipitating factor for some forms of epilepsy, although differential diagnosis between some seizure types and parasomnias may be difficult. Autosomal dominant frontal lobe epilepsy is characterized by nocturnal seizures with hyperkinetic automatisms and poorly organized stereotyped movements and has been associated with mutations of the α4 and β2 subunits of the neuronal nicotinic acetylcholine receptor. We performed a clinical and molecular genetic study of a large pedigree segregating sleep-related epilepsy in which seizures are associated with fear sensation, tongue movements, and nocturnal wandering, closely resembling nightmares and sleep …

AdultMalemedicine.medical_specialtyAdolescentSomnambulismMolecular Sequence DataMutation MissenseAutosomal dominant nocturnal frontal lobe epilepsyReceptors NicotinicBiologymedicine.disease_causeLigandsNicotinicArticleEpilepsyBIO/09 - FISIOLOGIAInternal medicineAcetylcholine; Adolescent; Adult; Aged; Aged 80 and over; Amino Acid Sequence; Epilepsy; Female; Humans; Ligands; Male; Molecular Sequence Data; Mutation Missense; Neurons; Pedigree; Receptors Nicotinic; Somnambulism; FearReceptorsmedicine80 and overGeneticsHumansIctalGenetics(clinical)Amino Acid SequenceGenetics (clinical)Acetylcholine receptorAgedAged 80 and overNeuronsMutationEpilepsySeizure typesFearmedicine.diseaseAcetylcholinePedigreeNicotinic acetylcholine receptorNicotinic agonistEndocrinologyMutationnAChR patch-clamp ADNFLE sleep-related epilepsy M1 TM1 ACh nicotineSettore MED/26 - NeurologiaFemaleMissense
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