Search results for "Pedigree"

showing 10 items of 313 documents

Progressive cerebellar ataxia, proximal neurogenic weakness and ocular motor disturbances: hexosaminidase A deficiency with late clinical onset in fo…

1997

Tay-Sachs disease is a genetically determined neurodegenerative disorder, resulting from mutations of the hexosaminidase (Hex) A gene coding for the alpha-subunit of beta-D-N-acetyl-hexosaminidase. Clinically, there is severe encephalomyelopathy leading to death within the first few years of life. Hex A activity is usually absent in tissue and body fluids of these patients. Juvenile and adult Hex A deficiencies are less severe but rare variants with some residual Hex A activity. All these variants are most prevalent among Ashkenazi Jews. We describe a non-Jewish family in which four adult brothers and sisters had markedly reduced Hex A activities and onset of symptoms in the second decade o…

AdultMalemedicine.medical_specialtyAtaxiaCerebellar AtaxiaEye MovementsBiopsyNeural ConductionCompound heterozygosityNuclear FamilyHexosaminidase AInternal medicinemedicineHumansHexosaminidaseAge of OnsetMotor Neuron DiseaseSkinMuscle WeaknessTay-Sachs Diseaseintegumentary systemTay-Sachs diseaseSpinal muscular atrophyDNAExonsmedicine.diseaseMagnetic Resonance ImagingAshkenazi jewsbeta-N-AcetylhexosaminidasesPedigreecarbohydrates (lipids)EndocrinologyPhenotypeNeurologyOculomotor MusclesCerebellar atrophyFemaleNeurology (clinical)Age of onsetmedicine.symptomPsychologyJournal of the neurological sciences
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Analysis of the gastrin-releasing peptide receptor gene in Italian patients with autism spectrum disorders

2008

The gastrin-releasing peptide receptor (GRPR) was implicated for the first time in the pathogenesis of Autism spectrum disorders (ASD) by Ishikawa-Brush et al. [Ishikawa-Brush et al. (1997): Hum Mol Genet 6: 1241-1250]. Since this original observation, only one association study [Marui et al. (2004): Brain Dev 26: 5-7] has further investigated, though unsuccessfully, the involvement of the GRPR gene in ASD. With the aim of contributing further information to this topic we have sequenced the entire coding region and the intron/exon junctions of the GRPR gene in 149 Italian autistic patients. The results of this study led to the identification of four novel point mutations, two of which, that…

AdultMalemedicine.medical_specialtyBALB 3T3 CellsAdolescentDNA Mutational AnalysisPopulationRett syndromeBiologyMiceCellular and Molecular NeuroscienceExonSettore BIO/13 - Biologia ApplicataInternal medicineGastrin-releasing peptideChlorocebus aethiopsmedicineGastrin-releasing peptide receptorAnimalsHumansPoint MutationAutistic DisorderChildautism gastrin-releasing peptide receptor signal transductionG-protein-coupled receptor association studyeducationGeneGenetics (clinical)AgedGeneticseducation.field_of_studyPoint mutationMiddle Agedmedicine.diseasePedigreeReceptors BombesinDevelopmental disorderPsychiatry and Mental healthEndocrinologyItalyCase-Control StudiesCOS CellsFemaleAmerican Journal of Medical Genetics Part B: Neuropsychiatric Genetics
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Franceschetti Hereditary Recurrent Corneal Erosion

2011

To describe new affected individuals of Franceschetti's original pedigree of hereditary recurrent erosion and to classify a unique entity called Franceschetti corneal dystrophy.Observational case series.Slit-lamp examination of 10 affected individuals was conducted. Biomicroscopic examinations were supplemented by peripheral corneal biopsy in 1 affected patient with corneal haze. Tissue was processed for light and electron microscopy and immunohistochemistry was performed. DNA analysis was carried out in 12 affected and 3 nonaffected family members.All affected individuals suffered from severe ocular pain in the first decade of life, attributable to recurrent corneal erosions. Six adult pat…

AdultMalemedicine.medical_specialtyBiopsyDNA Mutational AnalysisDermatan SulfateCorneal dystrophyCorneal OpacityCorneal erosionAntigens NeoplasmRecurrenceTransforming Growth Factor betaOphthalmologymedicineEye PainHumansChildAgedAged 80 and overCorneal Dystrophies HereditaryExtracellular Matrix Proteinsbusiness.industryCadherinsmedicine.diseaseImmunohistochemistryPedigreeRecurrent corneal erosionOphthalmologyClaudinsFemaleDecorinbusinessCell Adhesion MoleculesChondroitinBiomarkersAmerican Journal of Ophthalmology
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Clinical characteristics and determinants of the phenotype in TMEM43 arrhythmogenic right ventricular cardiomyopathy type 5.

2020

Arrhythmogenic right ventricular cardiomyopathy type V (ARVC-5) is the most aggressive heterozygous form of ARVC. It is predominantly caused by a fully penetrant mutation (p.S358L) in the nondesmosomal gene TMEM43-endemic to Newfoundland, Canada. To date, all familial cases reported worldwide share a common ancestral haplotype. It is unknown whether the p.S358L mutation by itself causes ARVC-5 or whether the disease is influenced by genetic or environmental factors. The purpose of this study was to examine the phenotype, clinical course, and the impact of exercise on patients with p.S358L ARVC-5 without the Newfoundland genetic background. We studied 62 affected individuals and 73 noncarrie…

AdultMalemedicine.medical_specialtyDNA Mutational AnalysisMutation MissenseDisease030204 cardiovascular system & hematologyVentricular Function LeftRight ventricular cardiomyopathySudden cardiac deathElectrocardiography03 medical and health sciences0302 clinical medicinePhysiology (medical)Internal medicinemedicineGeneticsHumans030212 general & internal medicineExerciseArrhythmogenic Right Ventricular DysplasiaEjection fractionTMEM43business.industryIncidence (epidemiology)HaplotypeMembrane ProteinsStroke VolumeDNAmedicine.diseasePhenotypePedigree3. Good healthPhenotypeMutation (genetic algorithm)CardiologyFemaleCardiology and Cardiovascular MedicinebusinessArrhythmogenic right ventricular cardiomyopathyArrhythmia
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Hereditary angioedema with normal C1-INH withversuswithout specificF12gene mutations

2015

Background Hereditary angioedema with normal C1-INH may be linked to specific mutations in the coagulation factor 12 (FXII) gene (HAE-FXII) or mutations in genes that are still unknown (HAE-unknown). To assess the differences in transmission and inheritance, clinical features, and laboratory parameters between patients with HAE-FXII and HAE-unknown. Methods Sixty-nine patients with HAE-FXII from 23 unrelated families and 196 patients with HAE-unknown from 65 unrelated families were studied. Results Both HAE-FXII and HAE-unknown are inherited as autosomal-dominant traits with incomplete penetrance. The male to female ratio was 1 : 68 in HAE-FXII and 1 : 6.3 in HAE-unknown. The maternal to pa…

AdultMalemedicine.medical_specialtyDatabases FactualOffspringImmunologyGene mutationSeverity of Illness IndexCohort StudiesYoung Adultchemistry.chemical_compoundAge DistributionInternal medicineHumansImmunology and AllergyMedicineHereditary Angioedema Type IIIAge of OnsetSex DistributionRetrospective Studiesmedicine.diagnostic_testAngioedemabusiness.industryIncidenceAngioedemas HereditaryMiddle AgedPrognosismedicine.diseasePenetranceRecombinant ProteinsPedigreePhenotypeEndocrinologychemistryPlasminogen activator inhibitor-1Factor XIIMutationHereditary angioedemaFemalemedicine.symptombusinessComplement C1 Inhibitor ProteinPartial thromboplastin timeAllergy
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Controversies and challenges in the management of chronic urticaria

2016

This supplement reports proceedings of the second international Global Urticaria Forum, which was held in Berlin, Germany in November 2015. Despite the clear international guideline, there remain a number of controversies and challenges in the management of patients with chronic urticaria (CU). As a result of major advancements in urticaria over the past 4 years, the current EAACI/GA(2) LEN/EDF/WAO urticaria guideline treatment algorithm requires updating. Case studies from patients with chronic spontaneous urticaria (CSU) [also called chronic idiopathic urticaria (CIU)], chronic inducible urticaria (CIndU) or diseases and syndromes related to CU are useful in describing and exploring chall…

AdultMalemedicine.medical_specialtyPathologyUrticariaAlternative medicineDermatologyUnmet needs030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicineimmune system diseasesparasitic diseasesmedicineHumansAngioedemaDisease management (health)ChildIntensive care medicineskin and connective tissue diseasesChronic urticariaAgedbusiness.industryGuidelineMiddle AgedPedigreeCold TemperatureInfectious Diseases030228 respiratory systemChronic DiseaseHistamine H1 AntagonistsSunlightFemaleChronic idiopathic urticariabusiness
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Increased Familial Clustering of Autoimmune Thyroid Diseases

2011

Data regarding familial prevalence and recurrence risk ratio of autoimmune thyroid diseases (AITD) in Germany are lacking. The data from 179 German families of AITD patients encompassing 1 229 relatives were collected using standardized clinical and laboratory diagnostic criteria. Of this large collective, 86 AITD index cases with their 139 children and 106 AITD index cases with their 157 siblings were included. The familial prevalence was estimated by the recurrence risk ratio. This quotient indicates whether first degree relatives display an increased risk for developing AITD, compared with the general population. AITD were present in 14 of children and 15 of siblings of patients with AIT…

AdultMalemedicine.medical_specialtyPediatricsAdolescentOffspringEndocrinology Diabetes and MetabolismClinical BiochemistryPopulationDiseaseBiochemistryThyroiditisYoung AdultEndocrinologyRisk FactorsGermanyInternal medicinePrevalencemedicineHumansYoung adultFamily historyFirst-degree relativeseducationAgededucation.field_of_studybusiness.industryBiochemistry (medical)ThyroidThyroiditis AutoimmuneGeneral MedicineMiddle Agedmedicine.diseasePedigreemedicine.anatomical_structureEndocrinologyFemalebusinessHormone and Metabolic Research
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Familial Occurrence of Inflammatory Bowel Disease in Celiac Disease

2003

BACKGROUND The authors have previously reported a possible increased risk of the familial occurrence of Crohn's disease in patients with celiac disease. AIM The aim of the current study was to evaluate in a case-control study the familial occurrence of inflammatory bowel disease (IBD) in first-degree relatives of patients with celiac disease. METHODS One hundred eleven consecutive patients with biopsy-proven celiac disease were interviewed to ascertain whether IBD was present in first-degree relatives. The number of relatives, their ages, and possible IBD status were collected in a questionnaire. When a diagnosis of familial IBD was reported, the diagnosis was checked in the hospital record…

AdultMalemedicine.medical_specialtyPopulationDiseaseGastroenterologyInflammatory bowel diseaseHospital recordsInternal medicinePrevalencemedicineHumansImmunology and AllergyIn patienteducationeducation.field_of_studybusiness.industryGastroenterologyCase-control studyInflammatory Bowel Diseasesmedicine.diseaseUlcerative colitisdigestive system diseasesPedigreeCeliac DiseaseIncreased riskCase-Control StudiesFemalebusinessInflammatory Bowel Diseases
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A Novel APOB Mutation Identified by Exome Sequencing Cosegregates With Steatosis, Liver Cancer, and Hypocholesterolemia

2013

Objective— In familial hypobetalipoproteinemia, fatty liver is a characteristic feature, and there are several reports of associated cirrhosis and hepatocarcinoma. We investigated a large kindred in which low-density lipoprotein cholesterol, fatty liver, and hepatocarcinoma displayed an autosomal dominant pattern of inheritance. Approach and Results— The proband was a 25-year-old female with low plasma cholesterol and hepatic steatosis. Low plasma levels of total cholesterol and fatty liver were observed in 10 more family members; 1 member was affected by liver cirrhosis, and 4 more subjects died of either hepatocarcinoma or carcinoma on cirrhosis. To identify the causal mutation in this f…

AdultMalemedicine.medical_specialtySettore MED/09 - Medicina InternaApolipoprotein BNonsense mutationBiologyArticlehypobetaliproteinemia type 1Hypobetalipoproteinemiasexome fatty liver hypobetalipoproteinemia familial 2Young Adultsymbols.namesakeInternal medicinemedicineHumansExomeHEPATOCELLULAR CARCINOMAExomeExome sequencingApolipoproteins Bfatty liverFamily HealthGeneticsSanger sequencingLiver NeoplasmsFatty liverMiddle AgedHEPATOCELLULAR CARCINOMA; exome; fatty liver; hypobetaliproteinemia type 1medicine.diseasePedigreeFatty LiverHypocholesterolemiaCholesterolEndocrinologyCodon Nonsensebiology.proteinsymbolsFemaleCardiology and Cardiovascular MedicineLiver cancerexomeArteriosclerosis, Thrombosis, and Vascular Biology
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Detection of a germline mutation and somatic homozygous loss of the von Hippel-Lindau tumor-suppressor gene in a family with a de novo mutation

1996

von Hippel-Lindau (VHL) disease is a pleiotropic disorder featuring a variety of malignant and benign tumors of the eye, central nervous system, kidney, and adrenal gland. Recently the VHL gene has been identified in the chromosomal region 3p25-26. Prognosis and successful management of VHL patients and their descendants depend on unambiguous diagnosis. Due to recurrent hemangioblastomas, a29-year-old patient without familial history of VHL disease was diagnosed to be at risk for the disease. Histopathological examination of a small renal mass identified a clear cell tumor with a G1 grading. Genetic characterization of the germline and of the renal tumor was performed. Polymerase chain reac…

AdultMalemedicine.medical_specialtyvon Hippel-Lindau DiseaseTumor suppressor geneDNA Mutational AnalysisMolecular Sequence Dataurologic and male genital diseasesPolymerase Chain ReactionGermlineGermline mutationVon Hippel–Lindau tumor suppressorGeneticsmedicineHumansGenes Tumor SuppressorSpinal Cord NeoplasmsVon Hippel–Lindau diseaseGerm-Line MutationPolymorphism Single-Stranded ConformationalGenetics (clinical)Sequence Deletionbiologymedicine.diagnostic_testHomozygoteCytogeneticsExonsmedicine.diseaseKidney Neoplasmsfemale genital diseases and pregnancy complicationsHemangioblastomaPedigreeKaryotypingChromosomal regionbiology.proteinCancer researchFemaleChromosomes Human Pair 3Chromosome DeletionFluorescence in situ hybridizationHuman Genetics
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