Search results for "Pedigree"

showing 10 items of 313 documents

Genetic background in nonalcoholic fatty liver disease: A comprehensive review

2015

In the Western world, nonalcoholic fatty liver disease (NAFLD) is considered as one of the most significant liver diseases of the twenty-first century. Its development is certainly driven by environmental factors, but it is also regulated by genetic background. The role of heritability has been widely demonstrated by several epidemiological, familial, and twin studies and case series, and likely reflects the wide inter-individual and inter-ethnic genetic variability in systemic metabolism and wound healing response processes. Consistent with this idea, genome-wide association studies have clearly identified Patatin-like phosholipase domain-containing 3 gene variant I148M as a major player i…

Genetic MarkersCandidate geneGenome-wide association studieHeredityPatatin-like phospholipase domain-containing 3Genome-wide association studyDiseaseReviewBiologymedicine.disease_causeGeneticNon-alcoholic Fatty Liver DiseaseRisk FactorsHeredityNonalcoholic fatty liver diseasemedicineHumansNonalcoholic fatty liver diseaseGenetic Predisposition to DiseaseGenetic variabilityGenetic associationGeneticsFatty liverGastroenterologyGenetic VariationGeneral Medicinemedicine.diseaseCandidate gene studiePedigreePhenotypeNonalcoholic steatohepatitiTransmembrane 6 superfamily member 2Candidate gene studies; Genetics; Genome-wide association studies; Nonalcoholic fatty liver disease; Nonalcoholic steatohepatitis; Patatin-like phospholipase domain-containing 3; Transmembrane 6 superfamily member 2Genome-Wide Association Study
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Fine mapping of the 2p11 dyslexia locus and exclusion of TACR1 as a candidate gene.

2003

Developmental dyslexia, or reading disability, is a multigenic complex disease for which at least five loci, i.e. DYX1-3 and DYX5-6, have been clearly identified from the human genome. To date, DYX1C1 is the only dyslexia candidate gene cloned. We have previously reported linkage to 2p11 and 7q32 in 11 Finnish pedigrees. Here, we report the fine mapping of the approximately 40-cM linked region from chromosome 2 as we increased marker density to one per 1.8 cM. Linkage was supported with the highest NPL score of 3.0 (P=0.001) for marker D2S2216. Association analysis using the six pedigrees showing linkage pointed to marker D2S286/rs3220265 (P value0.001) in the near vicinity of D2S2216. We w…

Genetic MarkersCandidate geneLocus (genetics)Quantitative trait locusBiologyPolymorphism Single NucleotideDyslexia03 medical and health sciences0302 clinical medicineGene mappingGenetic linkageGeneticsmedicineHumansGenetics (clinical)FinlandReceptors Tachykinin030304 developmental biologyGenetics0303 health sciencesGene Expression ProfilingHaplotypeDyslexiaChromosome Mappingmedicine.diseaseBlotting NorthernPedigreeGenetic markerChromosomes Human Pair 2030217 neurology & neurosurgeryMicrosatellite RepeatsHuman genetics
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Linkage studies of bipolar disorder in the region of the Darier's disease gene on chromosome 12q23-24.1.

1995

We have recently described a family in which there is cosegregation of major affective disorder with Darier's disease and have mapped this autosomal dominant skin disorder to 12q23-q24.1. This has provided an interesting candidate region for genetic studies of bipolar disorder. We have studied the segregation of seven markers spanning the Darier's disease locus in 45 bipolar disorder pedigrees and found modest evidence in support of linkage under heterogeneity for 5 of these markers. Nonparametric analyses were suggestive of linkage with a marker at the gene encoding a secretory form of phospholipase A2. Our sample has relatively low power to detect linkage under heterogeneity and independe…

Genetic MarkersMaleCandidate geneBipolar DisorderCosegregationGenotypeGenetic LinkageLocus (genetics)BiologyPhospholipases AGene mappingDarier DiseaseGenetic linkageDarier's diseasemedicineHumansBipolar disorderGenetics (clinical)AllelesGenes DominantGeneticsChromosomes Human Pair 12Chromosome Mappingmedicine.diseasePedigreePhospholipases A2FemaleLod ScoreDarier DiseaseAmerican journal of medical genetics
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An autosomal dominant retinitis pigmentosa family with close linkage to D7S480 on 7q.

1995

Retinitis pigmentosa is the most prevalent inherited disorder of the retina. It can be autosomal dominant (adRP), autosomal recessive (arRP) or X-linked (XLRP). A form of adRP mapping to chromosome 7q was reported in a large Spanish pedigree. We have typed DNA from the members of another Spanish family for polymorphic markers from the known candidate genes. Positive lod scores were obtained only for the markers located on 7q31-35, giving a maximum lod score of 2.98 (3.01 by multipoint analysis) at theta = 0.00 for D7S480. A brief clinical evaluation is given.

Genetic MarkersMaleCandidate genecongenital hereditary and neonatal diseases and abnormalitiesgenetic structuresBiologyAutosomal dominant retinitis pigmentosaGene mappingRetinitis pigmentosaGeneticsmedicineHumansGeneGenetics (clinical)Genes DominantLinkage (software)GeneticsChromosome Mappingmedicine.diseaseHuman geneticseye diseasesPedigreeGenetic markerFemaleLod ScoreChromosomes Human Pair 7Retinitis PigmentosaHuman genetics
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Linkage analysis in Usher syndrome type I (USH1) families from Spain.

1998

Usher syndrome (USH) is an autosomal recessive hereditary disorder characterised by congenital sensorineural hearing loss and gradual visual impairment secondary to retinitis pigmentosa (RP). The disorder is clinically and genetically heterogeneous. With regard to Usher type I (USH1), several subtypes have been described, the most frequent being USH1B located on chromosome 11q13.5. Of 18 USH1 families studied by linkage analysis, 12 (67%) showed significant lod score values for locus D11S527 (Zmax=14.032, theta=0.000) situated on chromosome 11q. Our findings suggest considerable genetic heterogeneity in the Spanish USH1 population. It is important to note that one of our families linked to …

Genetic MarkersMaleGenetic LinkageHearing Loss SensorineuralUsher syndromePopulationLocus (genetics)BiologyGenetic HeterogeneityGene mappingGenetic linkageRetinitis pigmentosaotorhinolaryngologic diseasesGeneticsmedicineHumanseducationGenetics (clinical)Geneticseducation.field_of_studyGenetic heterogeneityChromosomes Human Pair 11HaplotypeSyndromemedicine.diseaseeye diseasesPedigreeHaplotypesSpainFemaleRetinitis PigmentosaResearch ArticleJournal of Medical Genetics
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Mutations in the β-tropomyosin (TPM2) gene – a rare cause of nemaline myopathy

2002

Nemaline myopathy is a clinically and genetically heterogeneous muscle disorder. In the nebulin gene we have detected a number of autosomal recessive mutations. Both autosomal dominant and recessive mutations have been detected in the genes for alpha -actin and alpha -tropomyosin 3. A recessive mutation causing nemaline myopathy among the Old Order Amish has recently been identified in the gene for slow skeletal muscle troponin T. As linkage studies had shown that at least one further gene exists for nemaline myopathy, we investigated another tropomyosin gene expressed in skeletal muscle, the beta -tropomyosin 2 gene. Screening 66 unrelated patients, using single strand conformation polymor…

Genetic MarkersMaleGenetic LinkageProtein ConformationBiopsyMolecular Sequence DataMutation MissenseTropomyosinmacromolecular substancesMuscle disorderMyopathies NemalineTPM203 medical and health sciencesNebulin0302 clinical medicineNemaline myopathymedicineAnimalsHumansAmino Acid SequenceMuscle SkeletalNemaline bodiesPolymorphism Single-Stranded ConformationalGenetics (clinical)DNA Primers030304 developmental biologyGenetics0303 health sciencesSequence Homology Amino AcidbiologyReverse Transcriptase Polymerase Chain Reactionmusculoskeletal systemmedicine.diseaseMolecular biologyTropomyosinCongenital myopathyPedigree3. Good healthHaplotypesNeurologyMutationPediatrics Perinatology and Child Healthbiology.proteinFemaleNeurology (clinical)Sequence Alignment030217 neurology & neurosurgeryCentral core diseaseNeuromuscular Disorders
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Family studies in scleroderma (systemic sclerosis) demonstrating an HLA-linked increased chromosomal breakage rate in cultured lymphocytes

1988

An increased chromosomal breakage rate (ICBR) was found in 27 of 28 patients with scleroderma (systemic sclerosis, SS) - 5 with the syndrome including calcinosis cutis, Raynaud phenomenon, esophagus hypomotility, sclerodactyly and telangiectasia (CREST), 4 incomplete CREST, 1 overlapping syndrome, 18 progressive systemic sclerosis (PSS). Not only the patients, but also about half of their first-degree relatives showed an increased chromosomal breakage rate (more than 5 breaks per 100 metaphases). This character segregated as a dominant marker in nine families of scleroderma patients. In the six informative of the nine families, the ICBR trait showed close linkage with the HLA region on chro…

Genetic MarkersMaleSystemic diseaseGenetic LinkageHuman leukocyte antigenBiologySclerodermaCalcinosis cutisHLA AntigensGeneticsmedicineHumansLymphocytesCells CulturedGenetics (clinical)Chromosome AberrationsAutoimmune diseaseScleroderma SystemicSclerodactylyChromosome Fragilitymedicine.diseaseConnective tissue diseasePedigreeHaplotypesImmunologyFemalemedicine.symptomHuman Genetics
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Autosomal dominant polycystic kidney disease—in vitro culture of cyst-lining epithelial cells

1992

The major form of autosomal dominant polycystic kidney disease (ADPKD) in humans is linked to the PKD1 gene on chromosome 16p. The identity of the gene and the underlying pathogenetic mechanisms are not yet defined. Cyst-lining epithelial cells derived from a polycystic kidney were successfully grown in culture and designated MZ-PKD-1 cells. By linkage analysis, the related pedigree of the nephrectomized patient could be linked to the PKD1 gene on chromosome 16p. Thus, these cells exhibit the genotype of a mutated PKD1 gene and represent an in vitro culture model for ADPKD involving chromosome 16p. The antigenic phenotype was characterized immunohistologically by epithelial differentiation …

Genetic MarkersPathologymedicine.medical_specialtyAutosomal dominant polycystic kidney diseaseHLA-C AntigensBiologyEpitheliumGenetic linkagemedicineHumansNorthern blotGeneCells CulturedHLA-A AntigensPKD1urogenital systemAntibodies MonoclonalGeneral MedicineMiddle AgedBlotting NorthernPolycystic Kidney Autosomal Dominantmedicine.diseaseImmunohistochemistryMolecular biologyPhenotypePedigreeBlotMicroscopy ElectronPhenotypeHLA-B AntigensCell cultureFemaleChromosomes Human Pair 16Virchows Archiv B Cell Pathology Including Molecular Pathology
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Mutations in SLC20A2 link familial idiopathic basal ganglia calcification with phosphate homeostasis.

2012

Familial idiopathic basal ganglia calcification (IBGC) is a genetic condition with a wide spectrum of neuropsychiatric symptoms, including parkinsonism and dementia. Here, we identified mutations in SLC20A2, encoding the type III sodium-dependent phosphate transporter 2 (PiT2), in IBGC-affected families of varied ancestry, and we observed significantly impaired phosphate transport activity for all assayed PiT2 mutants in Xenopus laevis oocytes. Our results implicate altered phosphate homeostasis in the etiology of IBGC.

Genetic Markersmedicine.medical_specialtyGenetic LinkageMolecular Sequence DataMutation MissenseXenopusBasal ganglia calcification610 Medicine & healthPhosphates10052 Institute of PhysiologyXenopus laevis03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAsian PeopleBasal Ganglia Diseases1311 GeneticsCalcinosisGenetic linkageInternal medicineGeneticsmedicineAnimalsHomeostasisHumansBasal ganglia disease030304 developmental biology0303 health sciencesBase SequencebiologySodium-Phosphate Cotransporter Proteins Type IIIParkinsonismCalcinosisSequence Analysis DNAmedicine.diseasePhosphatebiology.organism_classificationPedigreeEndocrinologychemistry10076 Center for Integrative Human PhysiologyOocytes570 Life sciences; biologyLod Score030217 neurology & neurosurgeryHomeostasisChromosomes Human Pair 8Nature genetics
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Homozygous SMN1 exons 1-6 deletion: pitfalls in genetic counseling and general recommendations for spinal muscular atrophy molecular diagnosis.

2012

We report on a rare homozygous intragenic deletion encompassing exons 1-6 of the SMN1 gene in a patient with spinal muscular atrophy (SMA) born into a consanguineous family. This exceptional configuration induced misinterpretation of the molecular defect involved in this patient, who was first reported as having a classic SMN1 exon 7 deletion. This case points out the possible pitfalls in molecular diagnosis of SMA in affected patients and their relatives: exploration of the SMN1 exon 7 (c.840C/T alleles) may be disturbed by several non-pathological or pathological variants around the SMN1 exon 7. In order to accurately describe the molecular defect in an SMA-affected patient, we propose to…

Genetic counselingGenetic CounselingSMN1BiologyMuscular Atrophy SpinalExonGeneticsmedicineHumansAlleleGeneGenetics (clinical)AllelesGeneticsHomozygoteChromosome MappingInfantSpinal muscular atrophyExonsmedicine.diseaseSMA*Survival of Motor Neuron 1 Proteinnervous system diseasesPedigreeHuman genomeFemaleGene DeletionAmerican journal of medical genetics. Part A
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