Search results for " Pair 2"

showing 10 items of 55 documents

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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Prevalence of pathogenic copy number variants among children conceived by donor oocyte.

2021

AbstractDevelopment of assisted reproductive technologies to address infertility has favored the birth of many children in the last years. The majority of children born with these treatments are healthy, but some concerns remain on the safety of these medical procedures. We have retrospectively analyzed both the fertilization method and the microarray results in all those children born between 2010 and 2019 with multiple congenital anomalies, developmental delay and/or autistic spectrum disorder (n = 486) referred for array study in our center. This analysis showed a significant excess of pathogenic copy number variants among those patients conceived after in vitro fertilization with donor …

Male0301 basic medicineInfertilityDNA Copy Number VariationsReproductive Techniques AssistedMicroarraymedicine.medical_treatmentScienceDiseasesPrenatal diagnosisFertilization in VitroReproductive technologyBioinformaticsPolymorphism Single NucleotideRisk AssessmentArticle03 medical and health sciences0302 clinical medicineHuman fertilizationGeneticsPrevalenceHumansMedicineGenetic Predisposition to DiseaseCopy-number variationChild030219 obstetrics & reproductive medicineMultidisciplinaryIn vitro fertilisationMolecular medicinebusiness.industryQROocytemedicine.diseasePatologia030104 developmental biologymedicine.anatomical_structureRisk factorsChromosomes Human Pair 2KaryotypingOocytesMedicineFemalebusinessGenètica
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A de novo microdeletion of SEMA5A in a boy with autism spectrum disorder and intellectual disability.

2016

AbstractSemaphorins are a large family of secreted and membrane-associated proteins necessary for wiring of the brain. Semaphorin 5A (SEMA5A) acts as a bifunctional guidance cue, exerting both attractive and inhibitory effects on developing axons. Previous studies have suggested that SEMA5A could be a susceptibility gene for autism spectrum disorders (ASDs). We first identified a de novo translocation t(5;22)(p15.3;q11.21) in a patient with ASD and intellectual disability (ID). At the translocation breakpoint on chromosome 5, we observed a 861-kb deletion encompassing the end of the SEMA5A gene. We delineated the breakpoint by NGS and observed that no gene was disrupted on chromosome 22. We…

Male0301 basic medicinemedicine.medical_specialtyAutism Spectrum DisorderChromosomes Human Pair 22Translocation BreakpointNerve Tissue ProteinsSemaphorinsBiology[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsBioinformaticsArticleTranslocation GeneticautismeChromosome Breakpoints03 medical and health sciencesSemaphorin[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyIntellectual Disabilitymental disordersIntellectual disabilityGeneticsmedicineHumans[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsChildGenetics (clinical)Genetics[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyNeurosciencesMembrane Proteinsmedicine.disease030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutism spectrum disorderNeurons and CognitionPaternal InheritancecerveauChromosomes Human Pair 5AutismMedical geneticsChromosome DeletionmicrodélétionhumainChromosome 22[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyGenetic screen
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Soft tissue Ewing sarcoma--peripheral primitive neuroectodermal tumor with atypical clear cell pattern shows a new type of EWS-FEV fusion transcript.

2000

This study describes a new case of Ewing sarcoma (ES)-peripheral primitive neuroectodermal tumor (pPNET) with unusual phenotype and fusion gene structure. The tumor located in the inguinal area of a 15-year-old boy showed a highly aggressive behavior with hematogenous metastases after intensive chemotherapy and bone marrow transplant, causing death 28 months after diagnosis. The tumor displayed a clear cell pattern, and several neuroectodermal markers proved positive both in the original tumor and in xenografts. This neuroectodermal character was confirmed by electron microscopy. Moreover, cytogenetically the tumor has an unusual chromosomal rearrangement, t(2;22)(q13;q22,t(3;18)(p21;q23); …

MaleAdolescentOncogene Proteins FusionChromosomes Human Pair 22Transplantation HeterologousMice NudeSoft Tissue NeoplasmsChromosomal rearrangementSarcoma EwingBiologyGroinTranslocation GeneticPathology and Forensic MedicineFusion geneExonMiceFatal OutcomemedicineTumor Cells CulturedAnimalsHumansNeuroectodermal Tumors PrimitiveNeoplasm MetastasisMolecular BiologyPeripheral Primitive Neuroectodermal TumorReverse Transcriptase Polymerase Chain ReactionCell BiologyExonsmedicine.diseasePrognosisCombined Modality TherapyNeoplasm ProteinsFusion transcriptPrimitive neuroectodermal tumorChromosomes Human Pair 2KaryotypingCancer researchDisease ProgressionSarcomaClear cellDiagnostic molecular pathology : the American journal of surgical pathology, part B
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A genome screen for genes predisposing to bipolar affective disorder detects a new susceptibility locus on 8q

2001

Bipolar affective disorder (BPAD), also known as manic depressive illness, is a severe psychiatric disorder characterized by episodes of mania and depression. It has a lifetime prevalence of approximately 1% in all human populations. In order to identify chromosomal regions containing genes that play a role in determining susceptibility to this psychiatric condition, we have conducted a complete genome screen with 382 markers (average marker spacing of 9.3 cM) in a sample of 75 BPAD families which were recruited through an explicit ascertainment scheme. Pedigrees were of German, Israeli and Italian origin, respectively. Parametric and non-parametric linkage analysis was performed. The highe…

MaleBipolar DisorderGenotypePopulationPedigree chartLocus (genetics)BiologyNuclear FamilyVeinsGenomic ImprintingGenetic linkageLeukocytesGeneticsmedicineHumansGenetic Predisposition to DiseaseGenetic TestingBipolar disordereducationMolecular BiologyGenetics (clinical)Chromosomes Human Pair 14Geneticseducation.field_of_studyAutosomeChromosome MappingDNAGeneral Medicinemedicine.diseasePedigreePhenotypeChromosomes Human Pair 2FemaleLod Scoremedicine.symptomGenomic imprintingManiaChromosomes Human Pair 16Chromosomes Human Pair 8Microsatellite RepeatsHuman Molecular Genetics
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Amplification of ETS2 oncogene in acute nonlymphoblastic leukemia with t(6;21;18).

1992

Cytogenetic and molecular studies in a case of acute nonlymphoblastic leukemia (ANLL) are reported in this paper. Bone marrow blasts carried a hypodiploid karyotype with a complex t(6;18;21)(6qter----6p21::21q22----21qter;18qter ----18p11::6p22----6pter; 21pter----21q22::6p21----6p22::18p11----18pte r) and other numerical and structural changes. We studied the organization and the expression of the ETS2 gene which is located on chromosome 21 in order to investigate its possible involvement in the disease. DNA analysis showed a 20-fold amplification of ETS2 sequences; an increase of 3- to 4-fold in the mRNAs level compared to normal was shown by Northern hybridization.

MaleCancer ResearchChromosomes Human Pair 21Chromosomal translocationBiologyTranslocation GeneticProto-Oncogene Protein c-ets-2Proto-Oncogene ProteinsGene duplicationGeneticsmedicineHumansNorthern blotMolecular BiologySouthern blotAgedChromosome AberrationsOncogeneGene AmplificationKaryotypeProtein-Tyrosine KinasesBlotting NorthernMolecular biologyDNA-Binding ProteinsRepressor ProteinsBlotting SouthernLeukemia Myeloid Acutemedicine.anatomical_structureCancer researchTrans-ActivatorsChromosomes Human Pair 6Bone marrowChromosome 21Chromosomes Human Pair 18Transcription FactorsCancer genetics and cytogenetics
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“Masked” Philadelphia chromosome resulting from a t(X;22) in chronic myeloid leukemia

1988

Abstract A rare cytogenetic finding in chronic myeloid leukemia is reported. It consisted in a “masked” Philadelphia chromosome, resulting from an unusual translocation between chromosomes #22 and X. The t(X;22) was present in 100% of direct and cultured bone marrow cell preparations. Chromosome #9 did not seem to be involved in the formation of the Ph marker. Involvement of the X chromosome in karyotypic changes of hematologic diseases, with particular respect to chronic myeloid leukemia, is discussed.

MaleCancer Researchmedicine.medical_specialtyX ChromosomeChromosomes Human Pair 22Chromosomal translocationBiologyPhiladelphia chromosomeTranslocation Genetichemic and lymphatic diseasesGeneticsmedicineHumansPhiladelphia ChromosomeMolecular BiologyBone marrow cellX chromosomeGeneticsCytogeneticsMyeloid leukemiaChromosomeMiddle Agedmedicine.diseaseMolecular biologyLeukemia MyeloidKaryotypingCancer Genetics and Cytogenetics
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A genome scan for developmental dyslexia confirms linkage to chromosome 2p11 and suggests a new locus on 7q32

2003

Developmental dyslexia is a distinct learning disability with unexpected difficulty in learning to read despite adequate intelligence, education, and environment, and normal senses. The genetic aetiology of dyslexia is heterogeneous and loci on chromosomes 2, 3, 6, 15, and 18 have been repeatedly linked to it. We have conducted a genome scan with 376 markers in 11 families with 38 dyslexic subjects ascertained in Finland. Linkage of dyslexia to the vicinity of DYX3 on 2p was confirmed with a non-parametric linkage (NPL) score of 2.55 and a lod score of 3.01 for a dominant model, and a novel locus on 7q32 close to the SPCH1 locus was suggested with an NPL score of 2.77. The SPCH1 locus has p…

MaleCandidate geneGenotypeDNA Mutational AnalysisShort ReportLocus (genetics)BiologyDyslexia03 medical and health sciences0302 clinical medicineCommunication disorderDCDC2mental disordersGeneticsmedicineHumansLanguage disorderFinlandGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesGenome HumanDyslexiaChromosome MappingForkhead Transcription FactorsFOXP2medicine.diseasePedigreeRepressor ProteinsChromosomes Human Pair 2Learning disabilityFemaleLod Scoremedicine.symptomChromosomes Human Pair 7030217 neurology & neurosurgeryTranscription FactorsJournal of Medical Genetics
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The first case of myoclonic epilepsy in a child with a de novo 22q11.2 microduplication

2011

Chromosome 22, particularly the q11.2 sub-band, has long been recognized as responsible for multiple congenital anomaly disorders. In particular, its susceptibility to subtle microdeletions or, more rarely, microduplications has been attributed to the presence of several low-copy repeats spanning the region as mediators of nonallelic homologous recombination that result in 22q11.2 rearrangements. While recent data suggest that the frequency of 22q11.2 microduplications could be approximately half of all deletions, now only 50 unrelated cases have been reported thus far. However, it is reasonable to suppose that microduplications of 22q11.2 may be largely undetected as a result of a less-dis…

MaleChromosomes Human Pair 22Non-allelic homologous recombinationEpilepsies MyoclonicMultiple congenital anomalyBiologyRAB36 genemyoclonic epilepsySettore MED/38 - Pediatria Generale E SpecialisticaChromosome DuplicationGene duplicationClinical heterogeneityGeneticsmedicineHumansChildIn Situ Hybridization FluorescenceGenetics (clinical)GeneticsComparative Genomic HybridizationFaciesmedicine.diseaseMild learning difficultiesdevelopmental delayPhenotypeSettore MED/03 - Genetica MedicaChild PreschoolMyoclonic epilepsynonallelic homologous recombinationChromosome 2222q11.2 microduplicationComparative genomic hybridizationAmerican Journal of Medical Genetics Part A
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Additional evidence to support the role of the 20q13.33 region in susceptibility to autism

2012

MaleDNA Copy Number VariationsGenotypeChromosomes Human Pair 20MEDLINEReceptors NicotinicBiologyText miningKCNQ2 Potassium ChannelGenotypeGeneticsmedicineHumansKCNQ2 Potassium ChannelGenetic Predisposition to DiseaseAutistic DisorderChildGenetics (clinical)GeneticsComparative Genomic Hybridizationbusiness.industrymedicine.diseaseAutismChromosome DeletionbusinessComparative genomic hybridizationAmerican Journal of Medical Genetics Part A
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