Search results for " Mapping"

showing 10 items of 1411 documents

Evaluation of linkage of bipolar affective disorder to chromosome 18 in a sample of 57 German families.

1999

Previously reported linkage of bipolar affective disorder to DNA markers on chromosome 18 was reexamined in a large sample of German bipolar families. Twenty-three short tandem repeat markers were investigated in 57 families containing 103 individuals with bipolar I disorder (BPI), 26 with bipolar II disorder (BPII), nine with schizoaffective disorder of the bipolar type (SA/BP), and 38 individuals with recurrent unipolar depression (UPR). Evidence for linkage was tested with parametric and non-parametric methods under two definitions of the affected phenotype. Analysis of all 57 families revealed no robust evidence for linkage. Following previous reports we performed separate analyses afte…

Genetic MarkersMaleBipolar I disorderBipolar DisorderGenetic LinkageSchizoaffective disorderGenes RecessiveGenetic determinismNuclear FamilyCellular and Molecular NeuroscienceBipolar II disorderGenomic ImprintingChromosome 18GermanymedicineHumansFamilyBipolar disorderMolecular BiologyGenes DominantLinkage (software)GeneticsRecombination GeneticSex CharacteristicsModels GeneticChromosome Mappingmedicine.diseasePsychiatry and Mental healthChromosomal regionFemaleLod ScorePsychologyChromosomes Human Pair 18Molecular psychiatry
researchProduct

How to minimise the effect of tumour cell content in detection of aberrant genetic markers in neuroblastoma

2011

Background: Clinical heterogeneity reflects the complexity of genetic events associated with neuroblastoma (NB). To identify the status of all described genetic loci with possible prognostic interest, high-throughput approaches have been used, but only with tumour cell content >60%. In some tumours, necrotic, haemorrhagic and/or calcification areas influence the low amount of neuroblasts. We evaluated the effect of tumour cell content in the detection of relevant aberrant genetic markers (AGM) diagnosed by fluorescence in situ hybridisation (FISH) on tissue microarrays (TMA) in NB. Methods: Two hundred and thirty-three MYCN non-amplified primary NB included in 12 TMAs were analysed. Results…

Genetic MarkersMaleCancer ResearchPathologymedicine.medical_specialtyShort CommunicationCellBiologyneuroblastomaFISHaberrant genetic markersNeuroblastomatumour cell contentGene duplicationmedicineHumansNuclear proteinneoplasmsIn Situ Hybridization FluorescenceNeoplasm StagingOncogene ProteinsN-Myc Proto-Oncogene Proteinmedicine.diagnostic_testGene AmplificationChromosome MappingInfantNuclear Proteinsprognostic factorsCancerPrognosismedicine.diseaseSurvival Ratemedicine.anatomical_structureOncologyTissue Array AnalysisGenetic markerFemaleNeoplasm stagingFluorescence in situ hybridizationBritish Journal of Cancer
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

The copy number variant involving part of the α7 nicotinic receptor gene contains a polymorphic inversion.

2008

The alpha7 nicotinic acetylcholine receptor gene (CHRNA7) is located at 15q13-q14 in a region that is strongly linked to the P50 sensory gating deficit, an endophenotype of schizophrenia and bipolar disorder. Part of the gene is a copy number variant, due to a duplication of exons 5-10 and 3' sequence in CHRFAM7A, which is present in many but not all humans. Maps of this region show that the two genes are in opposite orientation in the individual mainly represented in the public access human DNA sequence database (Build 36), suggesting that an inversion had occurred since the duplication. We have used fluorescent in situ hybridization to investigate this putative inversion. Analysis of inte…

Genetic MarkersMaleLinkage disequilibriumBipolar DisorderPan troglodytesalpha7 Nicotinic Acetylcholine ReceptorReceptors NicotinicLinkage DisequilibriumExonGene duplicationGeneticsSettore MED/48 -Scienze Infermierist. e Tecn. Neuro-Psichiatriche e Riabilitat.AnimalsHumansCopy-number variationGeneSettore MED/25 - PsichiatriaGenetics (clinical)Sequence DeletionSegmental duplicationChromosomal inversionGeneticsChromosomes Human Pair 15Polymorphism GeneticBase SequencebiologyCHRNA7Chromosome Mappinginversion schizophrenia bipolar disorder 15q13–q14 CHRNA7 segmental duplicationChromosome InversionSchizophreniabiology.proteinFemale
researchProduct

Tetrasomy 18p de novo: Identification by FISH with conventional and microdissection probes and analysis of parental origin and formation by short seq…

1996

We report a de novo supernumerary isochromosome 18p in a child with tetrasomy 18p, analyzed by a straightforward combination of cytogenetic and molecular cytogenetic methods. The diagnostic procedure consisted of standard banding techniques and fluorescence in situ hybridization (FISH) with centromere and library DNA probes for chromosome 18, and 18p-specific FISH probes prepared by chromosome microdissection and in vitro amplification. The maternal origin as well as the most probable cell stages of formation of the supernumerary isochromosome were determined by typing of short sequence repeats (SSRs). The pattern of allelic distribution suggests a nondisjunction during meiosis followed by …

Genetic MarkersMalemedicine.medical_specialtyMarker chromosomeCentromereIsochromosomeMothersBiologyFathersTetrasomy 18pChromosome 18GeneticsmedicineHumansAllelesIn Situ Hybridization FluorescenceGenetics (clinical)Repetitive Sequences Nucleic AcidGeneticsmedicine.diagnostic_testCytogeneticsChromosome MappingInfantAneuploidymedicine.diseaseChromosome microdissectionMolecular biologyChild PreschoolTetrasomyFemaleChromosomes Human Pair 18DNA ProbesFluorescence in situ hybridizationHuman Genetics
researchProduct

Clinical relevance of polymorphic markers of arterial thrombosis.

1997

Case-control and cross-sectional studies show that some common molecular variations (polymorphisms) of genes coding for proteins involved in atherosclerosis and thrombosis are often present in subjects who have experienced cerebrovascular or cardiovascular events. The clinical impact of the majority of polymorphic markers is disputed by prospective reports. In contrast, their pathophysiological implications and their role in monitoring parameters that are difficult to be checked by alternative means, are documented by the large majority of the reports. From the evidence available, there may be suggestion for further impact of polymorphic markers in vascular medicine. To substantiate this, n…

Genetic MarkersPathologymedicine.medical_specialtyPolymorphism GeneticGenetic inheritanceArterial diseaseVascular diseasebusiness.industryChromosome MappingThrombosisHematologyPeptidyl-Dipeptidase Amedicine.diseaseBioinformaticsThrombosisIschemiaRisk FactorsGenetic markermedicineHumansClinical significanceProspective cohort studybusinessVascular Medicine
researchProduct

Comparative architectural aspects of regions of conserved synteny on human chromosome 11p15.3 and mouse chromosome 7 (including genes WEE1 and LMO1)

2001

Human chromosome 11p15.3 is associated with chromosome aberrations in the Beckwith Wiedemann Syndrome and implicated in the pathogenesis of different tumor types including lung cancer and leukemias. To date, only single tumor-relevant genes with linkage to this region (e.g. LMO1) have been found suggesting that this region may harbor additional potential disease associated genes. Although this genomic area has been studied for years, the exact order of genes/chromosome markers between D11S572 and the WEE1 gene locus remained unclear. Using the FISH technique and PAC clones of the flanking markers we determined the order of the genomic markers. Based on these clones we established a PAC cont…

Genetic Markerscongenital hereditary and neonatal diseases and abnormalitiesBeckwith–Wiedemann syndromeCell Cycle ProteinsBiologyChromosomesEvolution MolecularContig MappingMiceChromosome regionsGene OrderMetalloproteinsGeneticsmedicineAnimalsHumansCloning MolecularMolecular BiologyGeneConserved SequenceIn Situ Hybridization FluorescenceGenetics (clinical)Repetitive Sequences Nucleic AcidSyntenyOncogene ProteinsGeneticsChromosome 7 (human)Base CompositionChromosomes Human Pair 11Nuclear ProteinsChromosomeSequence Analysis DNALIM Domain ProteinsProtein-Tyrosine Kinasesmedicine.diseaseAT Rich SequenceGC Rich SequenceDNA-Binding ProteinsChromosome 3CpG IslandsChromosome 21Transcription FactorsCytogenetic and Genome Research
researchProduct

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
researchProduct