Search results for " Chromosomes"

showing 10 items of 59 documents

Preimplantation genetic diagnosis by fluorescence in situ hybridization: clinical possibilities and pitfalls.

2003

Preimplantation genetic diagnosis using the fluorescence in situ hybridization technique (FISH) is being used widely to prevent the transmission of sex-linked diseases, to screen for translocations, and for aneuploidy screenng in specific invitro fertilization (IVF) patient groups, along with FISH analysis of spematozoa in intertile men. In this study, we aim to critically analyze our clinical results in patients at risk of transmitting sex-linked diseases (n = 55), in carriers of translocations (n = 43), in women who have recurent miscarriage (two or more miscarriages) (n = 128), recurrent IVF failure (three or more failed IVF attempts) (n = 47), and patients of advanced maternal age (37 y…

Adultmedicine.medical_specialtyGenetic LinkagePregnancy High-RiskAneuploidyFertilization in VitroBiologyPreimplantation genetic diagnosisTranslocation GeneticMiscarriageRecurrent miscarriagemedicineHumansAdvanced maternal ageTreatment FailureIn Situ Hybridization FluorescencePreimplantation DiagnosisGynecologyPregnancySex Chromosomesmedicine.diagnostic_testIncidence (epidemiology)Genetic Diseases InbornObstetrics and Gynecologymedicine.diseaseAbortion SpontaneousFemaleFluorescence in situ hybridizationMaternal AgeJournal of the Society for Gynecologic Investigation
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Trefoil factor TFF1-induced protection of conjunctival cells from apoptosis at premitochondrial and postmitochondrial levels.

2008

PURPOSE. Goblet cells of the conjunctival epithelium synthesize and secrete TFF1 (Trefoil factor 1), a small protease-resistant peptide that, together with mucins, is responsible for the rheologic properties of the tear film. This study aimed to determine whether TFF1, whose synthesis increases in inflammatory conditions such as pterygium, could protect conjunctival cells from apoptosis. METHODS. Chang conjunctival cells, either wild-type or expressing TFF1 through stable transfection, were exposed to benzalkonium chloride (BAK) and ultraviolet (UV) irradiation to trigger apoptosis. The authors used cell fractionation to detect lipid raft‐associated proteins, coimmunoprecipitation to explor…

MESH : Cell LineMESH : Chromosomes Human Pair 21Chromosomes Human Pair 21CellApoptosisMESH: Flow CytometryMESH: Caspase 8Membrane Potentials0302 clinical medicineMESH: Mitochondrial MembranesMESH: Chromosomes Human Pair 21MESH : Membrane Potentials0303 health sciencesCaspase 8MESH : Caspase 8MESH : Benzalkonium CompoundsMESH : Tumor Suppressor ProteinsChromosome MappingFas receptorFlow CytometryXIAPMitochondriaMESH : Epithelial Cellsmedicine.anatomical_structureMESH: Epithelial Cells030220 oncology & carcinogenesisMitochondrial MembranesTrefoil Factor-1MESH : MitochondriaMESH : TransfectionBenzalkonium CompoundsConjunctivaMESH: Benzalkonium CompoundsProgrammed cell deathMESH: Enzyme ActivationMESH : ConjunctivaUltraviolet RaysMESH : Flow CytometryMESH: MitochondriaMESH: ConjunctivaCaspase 3BiologyInhibitor of apoptosisCaspase 8TransfectionCell Line03 medical and health sciencesMESH : Mitochondrial Membranesmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumansMESH: Membrane PotentialsMESH: Tumor Suppressor Proteins[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyMESH: HumansTumor Suppressor ProteinsMESH: ApoptosisMESH: TransfectionMESH : HumansEpithelial CellsMolecular biologyMESH: Cell LineEnzyme ActivationApoptosisMESH : Ultraviolet RaysMESH: Ultraviolet RaysMESH : Enzyme ActivationMESH: Chromosome MappingMESH : ApoptosisMESH : Chromosome Mapping
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Eradicating Mosquitoes using Translocations: a First Field Experiment

1972

THEORETICAL considerations have led to the assumption that chromosomal translocations with ensuing semisterility could be used to control pests1–3. Inversions could have the same effect in animals and plants in which crossing over occurs in both sexes4. Many translocations of different type and with various degrees of sterility have been produced in the mosquito Culex pipiens5–8. Preliminary laboratory experiments with these translocations have shown that a cage population can be diminished and finally exterminated after a few generations by the release of translocation heterozygotes into the population9.

Chromosome AberrationsMaleGeneticseducation.field_of_studyMosquito ControlSex ChromosomesMultidisciplinarybiologyEcologyCulexSterilityField experimentfungiPopulationChromosomal translocationbiology.organism_classificationChromosomal crossoverCulexMosquito controlAnimalsNatural enemieseducationNature
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Friedreich's Ataxia: Autosomal Recessive Disease Caused by an Intronic GAA Triplet Repeat Expansion

1996

International audience; Friedreich's ataxia (FRDA) is an autosomal recessive, degenerative disease that involves the central and peripheral nervous systems and the heart. A gene, X25, was identified in the critical region for the FRDA locus on chromosome 9q13. This gene encodes a 210-amino acid protein, frataxin, that has homologs in distant species such as Caenorhabditis elegans and yeast. A few FRDA patients were found to have point mutations in X25, but the majority were homozygous for an unstable GAA trinucleotide expansion in the first X25 intron.

MaleIron-sulfur cluster assemblyPolymerase Chain Reaction0302 clinical medicineTrinucleotide RepeatsIron-Binding ProteinsGenetics0303 health sciencesMultidisciplinaryAutosomal recessive cerebellar ataxiaPedigree3. Good healthFemalemedicine.symptomChromosomes Human Pair 9HumanPair 9Heterozygotecongenital hereditary and neonatal diseases and abnormalitiesAtaxiaMolecular Sequence DataGenes RecessiveLocus (genetics)BiologyChromosomes03 medical and health sciencesGene mappingAlleles; Amino Acid Sequence; Base Sequence; Chromosomes Human Pair 9; DNA Primers; Female; Friedreich Ataxia; Genes Recessive; Heterozygote; Humans; Male; Molecular Sequence Data; Pedigree; Point Mutation; Polymerase Chain Reaction; Proteins; Sequence Alignment; Introns; Iron-Binding Proteins; Trinucleotide RepeatsmedicineRecessiveHumansPoint MutationAmino Acid SequenceAlleleAllelesDNA Primers030304 developmental biologyBase SequencePoint mutationProteins[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologymedicine.diseaseMolecular biologyIntronsGenes[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsFriedreich AtaxiaFrataxinbiology.proteinSequence Alignment030217 neurology & neurosurgeryScience
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Sex reversal from functional disomy of Xp: Prenatal and post-mortem findings.

2008

Translocations involving the short arms of the X and Y chromosomes are uncommon and are often associated with anomalies in gonadal development. Segmental duplications of the X chromosome interfere with the formation of the testis in patients with a 46,XY karyotype. The gene products located within the duplicated segment, when present in double dose, may affect on male sex development. We report on a fetus with karyotype 46,XY,der (14)t(X;14) (p10;p10)dn. Attached to chromosome 14 is the entire short arm of the X chromosome. Therefore, the fetus is affected with a disomy of Xp, resulting in complete male to female sex reversal, as well as other structural defects. To the best of our knowledg…

Malesex severalDisorders of Sex DevelopmentChromosomal translocationBiologysex reversal • Xp disomy • DAX1 gene • multiple congenital anomaliesTranslocation GeneticChromosome PaintingSettore MED/38 - Pediatria Generale E SpecialisticaPregnancyPrenatal DiagnosisGene duplicationGeneticsHumansAbnormalities MultipleGenetics (clinical)X chromosomeSex Chromosome AberrationsSegmental duplicationUltrasonographyGeneticsChromosome AberrationsChromosomes Human Pair 14FetusChromosomes Human XSex ChromosomesInfant NewbornChromosomeKaryotypeSex reversalChromosome BandingPhenotypeSettore MED/03 - Genetica MedicaKaryotypingTetralogy of FallotFemaledisomy XpDandy-Walker Syndrome
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Interstitial deletions of chromosome 1p: novel 1p31.3p22.2 microdeletion in a newborn with craniosynostosis, coloboma and cleft palate, and review of…

2022

Abstract Background Rearrangements of unstable DNA sequences may alter the structural integrity or the copy number of dose-sensitive genes, resulting in copy number variations. They may lead more frequently to deletions, in addition to duplications and/or inversions, which are the underlying pathogenic mechanism of a group of conditions known as genomic disorders (or also contiguous gene syndromes). Interstitial deletions of the short arm of chromosome 1 are rare, and only about 30 patients have been reported. Their clinical features are variable, in respect of the extent of the deleted region. They include global developmental delay, central nervous system (CNS) malformations, craniosynost…

Cleft PalateColobomaComparative Genomic HybridizationCraniosynostosesPhenotypeDNA Copy Number VariationsChromosomes Human Pair 1HumansFemaleGenomicsChromosome Deletion1p31.1 deletion syndrome Array-CGH Case report Chromosome 1 Contiguous gene syndrome Chromosome Deletion Chromosomes Human Pair 1 Comparative Genomic Hybridization DNA Copy Number Variations Female Genomics Humans Phenotype Cleft Palate Coloboma Craniosynostoses
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Analysis of t(15;17) chromosomal breakpoint sequences in therapy-related versus de novo acute promyelocytic leukemia: Association of DNA breaks with …

2010

We compared genomic breakpoints at the PML and RARA loci in 23 patients with therapy-related acute promyelocytic leukemia (t-APL) and 25 de novo APL cases.Eighteen of 23 t-APL cases received the topoisomerase II poison mitoxantrone for their primary disorder. DNA breaks were clustered in a previously reported 8 bp "hot spot" region of PML corresponding to a preferred site of mitoxantrone-induced DNA topoisomerase II-mediated cleavage in 39% of t-APL occurring in patients exposed to this agent and in none of the cases arising de novo (P = 0.007). As to RARA breakpoints, clustering in a 3' region of intron 2 (region B) was found in 65% of t-APL and 28% of de novo APL patients, respectively. S…

MaleCancer ResearchReceptors Retinoic AcidRetinoic AcidMessengerPromyelocytic Leukemia ProteinTranslocation GeneticChromosome BreakpointsLeukemia Promyelocytic Acuteimmune system diseasesReceptorsPromyelocyticGeneticsLeukemiabiologyReverse Transcriptase Polymerase Chain ReactionRetinoic Acid Receptor alphaNuclear ProteinsDNA NeoplasmMiddle AgedFemaleHumanAdultAcute promyelocytic leukemiaChromosome BreakpointsTranslocationAntineoplastic AgentsAcuteChromosomesYoung AdultPromyelocytic leukemia proteinGeneticGeneticsmedicineConsensus sequenceHumansRNA MessengerReceptors Retinoic Acid; Male; Young Adult; Middle Aged; Chromosome Breakpoints; Female; Chromosomes Human Pair 17; Tumor Suppressor Proteins; Humans; DNA Neoplasm; Translocation Genetic; Leukemia Promyelocytic Acute; Antineoplastic Agents; Nuclear Proteins; RNA Messenger; Mitoxantrone; Reverse Transcriptase Polymerase Chain Reaction; Chromosomes Human Pair 15; Transcription Factors; Aged; AdultneoplasmsAgedChromosomes Human Pair 15Pair 17Tumor Suppressor ProteinsTopoisomeraseBreakpointPair 15DNAmedicine.diseaseRetinoic acid receptor alphabiology.proteinNeoplasmRNAHuman genomeMitoxantroneSettore MED/15 - Malattie del SangueChromosomes Human Pair 17Transcription FactorsGenes, Chromosomes and Cancer
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A follow-up study of a genome-wide association scan identifies a susceptibility locus for venous thrombosis on chromosome 6p24.1.

2010

International audience; To identify genetic susceptibility factors conferring increased risk of venous thrombosis (VT), we conducted a multistage study, following results of a previously published GWAS that failed to detect loci for developing VT. Using a collection of 5862 cases with VT and 7112 healthy controls, we identified the HIVEP1 locus on chromosome 6p24.1 as a susceptibility locus for VT. Indeed, the HIVEP1 rs169713C allele was associated with an increased risk for VT, with an odds ratio of 1.20 (95% confidence interval 1.13-1.27, p = 2.86 x 10(-9)). HIVEP1 codes for a protein that participates in the transcriptional regulation of inflammatory target genes by binding specific DNA …

MESH : Transcription Factors[SDV]Life Sciences [q-bio]Genome-wide association study030204 cardiovascular system & hematologyMESH : Chromosomes Human Pair 60302 clinical medicineGenetics(clinical)Genetics (clinical)GeneticsVenous Thrombosis0303 health sciencesMESH: Polymorphism Single NucleotideMESH : Polymorphism Single NucleotideMESH: Genetic Predisposition to DiseaseMESH: Follow-Up StudiesMESH: Transcription FactorsMESH : Venous ThrombosisMESH: Case-Control StudiesDNA-Binding ProteinsChromosomes Human Pair 6MESH : DNA-Binding ProteinsErratumMESH : Genome-Wide Association StudyMESH : Case-Control StudiesMESH: Chromosomes Human Pair 6Locus (genetics)BiologyPolymorphism Single NucleotideGenetic determinism03 medical and health sciencesReportGenetic predispositionGeneticsHumansGenetic Predisposition to DiseaseAlleleGene030304 developmental biologyMESH: Humans[ SDV ] Life Sciences [q-bio]MESH : Humanslinking inflammation protein atherothrombosis sequence riskCase-control studyChromosomeMESH : Follow-Up StudiesCase-Control StudiesMESH: Genome-Wide Association StudyMESH: Venous ThrombosisMESH : Genetic Predisposition to Disease030217 neurology & neurosurgeryMESH: DNA-Binding ProteinsFollow-Up StudiesGenome-Wide Association StudyTranscription Factors
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Association of a functional deficit of the BKCa channel, a synaptic regulator of neuronal excitability, with autism and mental retardation

2006

International audience; Objective: Autism is a complex, largely genetic psychiatric disorder. In the majority of cases, the cause of autism is not known, but there is strong evidence for a genetic etiology. To identify candidate genes, the physical mapping of balanced chromosomal aberrations is a powerful strategy, since several genes have been characterized in numerous disorders. In this study, the authors analyzed a balanced reciprocal translocation arising de novo in a subject with autism and mental retardation. Method: The authors performed the physical mapping of the balanced 9q23/ 10q22 translocation by fluorescent in situ hybridization experiments using bacterial artificial chromosom…

MaleCandidate geneChromosomes Artificial BacterialIndolesDNA Mutational AnalysisRegulatorChromosomal translocationautism mental retardation KCNMA1 genelarge conductance Ca(2+)-activated K(+) (BK(Ca)) channel synaptic transmission chromosomal translocationSynaptic TransmissionTranslocation GeneticPair 10CA2+-ACTIVATED K+ CHANNELSCloning MolecularChildLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMUTATIONIn Situ HybridizationIn Situ Hybridization FluorescenceReverse Transcriptase Polymerase Chain ReactionBacterialChromosome MappingETIOLOGYPsychiatry and Mental healthArtificialKCNMA1 Gene[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]HaploinsufficiencyPsychologyChromosomes Human Pair 9POTASSIUM CHANNELSHumanPair 9Autistic Disorder; Child; Chromosome Aberrations; Chromosome Mapping; Chromosomes; Artificial; Bacterial; Chromosomes; Human; Pair 10; Chromosomes; Human; Pair 9; Cloning; Molecular; DNA Mutational Analysis; Humans; In Situ Hybridization; Fluorescence; Indoles; Intellectual Disability; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits; Male; Reverse Transcriptase Polymerase Chain Reaction; Synaptic Transmission; Translocation; GeneticTranslocationNeurotransmissionChromosomesFluorescenceGeneticIntellectual DisabilitymedicineHumansAutistic DisorderRELEASEChromosome AberrationsCOMPLEXChromosomes Human Pair 10MolecularAutistic Disorder; Child; Chromosome Aberrations; Chromosome Mapping; Chromosomes Artificial Bacterial; Chromosomes Human Pair 10; Chromosomes Human Pair 9; Cloning Molecular; DNA Mutational Analysis; Humans; In Situ Hybridization Fluorescence; Indoles; Intellectual Disability; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits; Male; Reverse Transcriptase Polymerase Chain Reaction; Synaptic Transmission; Translocation GeneticPERVASIVE DEVELOPMENTAL DISORDERSmedicine.diseaseDevelopmental disorderINDIVIDUALSLARGE-CONDUCTANCEAutismSCREENNeuroscience[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyCloning
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Population structure in the Méditerranean basin: a Y chromosome perspective

2006

The Mediterranean region has been characterised by a number of pre-historical and historical demographic events whose legacy on the current genetic landscape is still a matter of debate. In order to investigate the degree of population structure across the Mediterranean, we have investigated Y chromosome variation in a large dataset of Mediterranean populations, 11 of which are first described here. Our analyses identify four main clusters in the Mediterranean that can be labelled as North Africa, Arab, Central-East and West Mediterranean. In particular, Near Eastern samples tend to separate according to the presence of Arab Y chromosome lineages, suggesting that the Arab expansion played a…

Mediterranean climateMaledemographyhaplotypeSouthern EuropegenotypeUEPsPopulation geneticsVariation (Genetics)ArabMediterraneanMediterranean BasinArab; article; cluster analysis; demography; gene locus; genetic linkage; genetic variability; genotype; haplotype; human; male; North Africa; population genetics; population structure; priority journal; Southern Europe; Y chromosome Chromosomes Human Y; Ethnic Groups; Genetics Population; Humans; Male; Mediterranean Region; Variation (Genetics)genetic linkagegenetic variabilityEthnicity[SDV.BDD]Life Sciences [q-bio]/Development BiologyGenetics (clinical)Genetics0303 health scienceseducation.field_of_studyEcologyMediterranean Region030305 genetics & heredityarticlepriority journalMediterranean; Population genetic structure; STRs; UEPs; Y chromosomeY-chromosome population genetics ArabYgene locusPopulationPopulationEthnic GroupsBiologyY chromosomeChromosomes03 medical and health sciencesGenetic variationGeneticsHumansPopulation genetic structureGenetic variabilityhumaneducation030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsChromosomes Human YY chromosomeHaplotypeGenetic Variationpopulation geneticspopulation structureSettore MED/43 - MEDICINA LEGALENorth AfricaSettore BIO/18 - GeneticaGenetics PopulationSTRscluster analysis
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