Search results for "Chromosomes"

showing 10 items of 509 documents

The HTR1B 861GC receptor polymorphism among patients suffering from alcoholism, major depression, anxiety disorders and narcolepsy.

2000

Abstract The HTR1B receptor gene has been linked to antisocial alcoholism in a Finnish population and an American Indian tribe [Lappalainen et al., Arch. Gen. Psychiatry, 55 (1998) 989]. Using a candidate gene approach, we genotyped 209 patients with alcoholism, 108 patients with major depression, 32 patients with panic disorder, 50 patients with generalized anxiety disorder, 58 patients with narcolepsy and 74 healthy volunteers for the HTR1B 861G>C polymorphism. There was a higher frequency of the HTR1B 861G alleles among the alcohol-dependent patients as compared to the control subjects (χ 2 =4.02, d.f.=2, P =0.04). However, the association resulted from higher frequencies of the opposite…

AdultMaleRiskCandidate genemedicine.medical_specialtyGeneralized anxiety disorderGenotypeInternal medicineGermanymedicineHumansPsychiatryTemperamentBiological PsychiatryPsychiatric geneticsAllelesNarcolepsyDepressive Disorder MajorPolymorphism GeneticPanic disorderPanicmedicine.diseaseAnxiety DisordersPsychiatry and Mental healthAlcoholismPhenotypeCase-Control StudiesReceptors SerotoninReceptor Serotonin 5-HT1BAnxietyPanic DisorderChromosomes Human Pair 6Femalemedicine.symptomPsychologyAnxiety disorderNarcolepsyPsychiatry research
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Risk gene variants for nicotine dependence in the CHRNA5-CHRNA3-CHRNB4 cluster are associated with cognitive performance

2010

Recent studies strongly support an association of the nicotinic acetylcholine receptor gene cluster CHRNA5-CHRNA3-CHRNB4 with nicotine dependence (ND). However, the precise genotype-phenotype relationship is still unknown. Clinical and epidemiological data on smoking behavior raise the possibility that the relevant gene variants may indirectly contribute to the development of ND by affecting cognitive performance in some smokers who consume nicotine for reasons of "cognition enhancement." Here, we tested seven single nucleotide polymorphisms (SNPs) rs684513, rs637137, rs16969968, rs578776, rs1051730, rs3743078, rs3813567 from the CHRNA5-CHRNA3-CHRNB4 gene cluster for association with ND, me…

AdultMaleRiskGenotypeGene ExpressionNerve Tissue ProteinsSingle-nucleotide polymorphismReceptors NicotinicBiologyBioinformaticsPolymorphism Single NucleotideNicotineCellular and Molecular NeuroscienceCognitionGene clustermedicineHumansGenetic Predisposition to DiseaseRNA MessengerRisk factorAlleleGenetic Association StudiesGenetics (clinical)AgedGeneticsChromosomes Human Pair 15Gene Expression ProfilingCHRNA5HaplotypeWechsler ScalesGenetic VariationCognitionTobacco Use DisorderMiddle AgedPsychiatry and Mental healthMultigene Familybiology.proteinFemalemedicine.drugAmerican Journal of Medical Genetics Part B: Neuropsychiatric Genetics
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Smoking habits of parents and male: female ratio in spermatozoa and preimplantation embryos

2005

BACKGROUND Previous observations have addressed a decreased male:female ratio associated with smoking. Our aim was to assess whether this effect is observed at the spermatozoa or at the early embryo development. METHODS We retrospectively assessed smoking intake habits of 56 couples included in our preimplantation genetic diagnosis (PGD) program. Three groups were established according to male or female cigarette consumption per day: non-smokers, smokers (1-19 cigarettes per day) and heavy smokers (> or =20 cigarettes per day). Fluorescence in-situ hybridization (FISH) was performed on ejaculated sperm samples to analyse chromosomes X and Y. On day 3, embryos were also analysed. Additionall…

AdultMaleSemenBiologyPreimplantation genetic diagnosisAndrologyPregnancyCapacitationmedicineHumansSex RatioIn Situ Hybridization FluorescenceRetrospective StudiesChromosomes Human XChromosomes Human Ymedicine.diagnostic_testIncidenceIncidence (epidemiology)SmokingRehabilitationObstetrics and GynecologyEmbryoSpermatozoaSpermBlastocystReproductive MedicineFemaleSex ratioFluorescence in situ hybridizationHuman Reproduction
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Sleep disturbances in Angelman syndrome: a questionnaire study.

2003

Only few studies are available on sleep disorders in Angelman syndrome (AS), a neurodevelopmental disorder with several behavior disturbances. The aim of this study was to determine the prevalence of sleep disorders in a relatively large group of AS subjects, compared to that of age-matched controls. Forty-nine consecutive parents of patients with AS (26 males and 23 females aged 2.3-26.2 years) were interviewed and filled out a comprehensive sleep questionnaire. Based on their genetic etiology, four groups were defined: deletion of chromosome 15q11-13 (25 subjects); methylation imprinting mutation (six subjects), UBE3A mutations (seven subjects) and paternal uniparental disomy (five subjec…

AdultMaleSleep Wake DisordersPediatricsmedicine.medical_specialtyAdolescentUbiquitin-Protein LigasesComorbidityNeurodevelopmental disorderDevelopmental NeuroscienceReference ValuesAngelman syndromeSurveys and QuestionnairesmedicineUBE3APrevalenceHumansWakefulnessPsychiatryChildangelman syndrome; questionnaire study; sleep disordersSleep disorderChromosomes Human Pair 15questionnaire studySleep terrorAge FactorsGeneral MedicineSomnambulismDNA MethylationUniparental Disomymedicine.diseaseSleep in non-human animalsItalyChild PreschoolPediatrics Perinatology and Child HealthMutationsleep disordersFemaleNeurology (clinical)Sleep onsetAngelman SyndromePsychologySleepBraindevelopment
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Influence of sex and genetic variability on expression of X-linked genes in human monocytes

2011

Abstract In humans, the fraction of X-linked genes with higher expression in females has been estimated to be 5% from microarray studies, a proportion lower than the 25% of genes thought to escape X inactivation. We analyzed 715 X-linked transcripts in circulating monocytes from 1,467 subjects and found an excess of female-biased transcripts on the X compared to autosomes (9.4% vs 5.5%, p  −5 ). Among the genes not previously known to escape inactivation, the most significant one was EFHC2 whose 20% of variability was explained by sex. We also investigated cis expression quantitative trait loci (eQTLs) by analyzing 15,703 X-linked SNPs. The frequency and magnitude of X-linked cis eQTLs were…

AdultMaleTranscription GeneticMicroarrayQuantitative Trait LociSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideMonocytesX-inactivationSex FactorsGenes X-LinkedX Chromosome InactivationGene expressionGeneticsHumansGenetic variabilityGeneAgedGeneticsChromosomes Human XAutosomeCalcium-Binding ProteinsGenderGenetic VariationMiddle AgedExpression Quantitative Trait LocusExpression quantitative trait lociFemaleGene expressionGenome-Wide Association StudyGenomics
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High incidence of chromosomal abnormalities in large-headed and multiple-tailed spermatozoa

2006

Rodrigo Vivo, Lorena, lorovi@alumni.uv.es ; Prados Dodd, Nicolas, Nicolas.Prados@uv.es ; Gil Salom, Manuel Luis, Manuel.Gil-Salom@uv.es ; Remohi Gimenez, Jose Alejandro, J.Alejandro.Remohi@uv.es

AdultMaleUrologyEndocrinology Diabetes and Metabolismmedia_common.quotation_subjectLarge-HeadedPhysiologyBiologyEndocrinology:CIENCIAS MÉDICAS ::Medicina interna [UNESCO]Chromosomes HumanHumansIn Situ Hybridization Fluorescencemedia_commonUNESCO::CIENCIAS MÉDICAS ::Medicina internaChromosome AberrationsIncidenceChromosomal AbnormalitiesIncidence (epidemiology)Germinal cellAnatomy:CIENCIAS MÉDICAS [UNESCO]Reproductive MedicineIncidence ; Chromosomal Abnormalities ; Large-Headed ; Multiple-Tailed SpermatozoaKaryotypingSperm TailUNESCO::CIENCIAS MÉDICASSperm HeadHigh incidenceMultiple-Tailed SpermatozoaReproduction
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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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Two complementary recombinant chromosomes 5 in a healthy woman

2005

We report a healthy woman with two abortions who is a carrier for a rare heterozygous double recombinant of an inv(5) chromosome, karyotype 46,XX,rec(5)dup(5p) inv(5)(pl 3q22),rec(5)dup(5q)inv(5)(pl 3q22). Her father had a 46,XY,inv(5)(p13q22) karyotype; his consanguineous wife had died. Molecular investigation of 11 highly polymorphic markers spanning chromosome 5 revealed biparental inheritance for two markers (D5S406, D5S681) on 5p15.3 and 5q13.1, and an allele constellation not compatible with paternal heterodisomy for marker D5S623 on 5q11.2. Eight markers were not informative. Three mechanisms of formation are proposed: First, fertilization of a normal oocyte by a sperm carrying the t…

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesAbortion HabitualDNA RecombinantBiologylaw.inventionPolymorphism (computer science)lawGeneticsHumansBase sequenceMolecular BiologyGenetics (clinical)Polymorphism GeneticBase SequenceChromosomeKaryotypebiochemical phenomena metabolism and nutritionMolecular biologyHealthKaryotypingdupChromosome InversionRecombinant DNAbacteriaChromosomes Human Pair 5Female
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Epimutation at human chromosome 14q32.2 in a boy with a upd(14)mat-like clinical phenotype.

2009

Recently, three reports described deletions and epimutations affecting the imprinted region at chromosome 14q32.2 in individuals with a phenotype typical for maternal uniparental disomy of chromosome 14 [upd(14)mat]. In this study, we describe another patient with upd(14)mat-like phenotype including low birth weight, neonatal feeding problems, muscular hypotonia, motor and developmental delay, small hands and feet, and truncal obesity. Conventional cytogenetic analyses, fluorescence in situ hybridization subtelomere screening, multiplex ligation-dependent probe amplification analysis of common microdeletion and microduplication syndromes, and methylation analysis of SNRPN all gave normal re…

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesMolecular Sequence DataMothersBiologyMethylationPolymorphism Single NucleotideEpigenesis GeneticGenomic ImprintingIntergenic regionGeneticsmedicineHumansAbnormalities MultipleEpigeneticsChildGenetics (clinical)GeneticsChromosomes Human Pair 14Muscular hypotoniamedicine.diagnostic_testBase SequenceChromosomeUniparental DisomySubtelomerePhenotypeDifferentially methylated regionsPhenotypeMutationFemaleFluorescence in situ hybridizationClinical genetics
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Two independent chromosomal rearrangements, a very small (550 kb) duplication of the 7q subtelomeric region and an atypical 17q11.2 <i>(NF1)&lt…

2006

Most patients with neurofibromatosis (NF1) are endowed with heterozygous mutations in the <i>NF1</i> gene. Approximately 5% show an interstitial deletion of chromosome 17q11.2 (including <i>NF1</i>) and in most cases also a more severe phenotype. Here we report on a 7-year-old girl with classical NF1 signs, and in addition mild overgrowth (97th percentile), relatively low OFC (10th–25th percentile), facial dysmorphy, hoarse voice, and developmental delay. FISH analysis revealed a 17q11.2 microdeletion as well as an unbalanced 7p;13q translocation leading to trisomy of the 7q36.3 subtelomeric region. The patient’s mother and grandmother who were phenotypically normal …

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesNeurofibromatosesmedia_common.quotation_subjectBiologyCytogeneticsGene DuplicationGene duplicationGeneticsmedicineHumansGirlNeurofibromatosisneoplasmsMolecular BiologyGeneIn Situ Hybridization FluorescenceGenetics (clinical)Oligonucleotide Array Sequence AnalysisNeurofibromatosesmedia_commonGeneticsInfantChromosomeTelomereSubtelomeremedicine.diseaseeye diseasesnervous system diseasesChild PreschoolFemaleChromosome DeletionChromosomes Human Pair 7Chromosomes Human Pair 17Cytogenetic and Genome Research
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