Search results for "Chromosomes"

showing 10 items of 509 documents

NF1 microdeletion syndrome: case report of two new patients

2019

Abstract Background 17q11.2 microdeletions, which include the neurofibromatosis type 1 (NF1) gene region, are responsible for the NF1 microdeletion syndrome, observed in 4.2% of all NF1 patients. Large deletions of the NF1 gene and its flanking regions are associated with a more severe NF1 phenotype than the NF1 general population. Case presentation We hereby describe the clinical and molecular features of two girls (aged 2 and 4 years, respectively), with non-mosaic atypical deletions. Patient 1 showed fifteen café-au-lait spots and axillary freckling, as well as a Lisch nodule in the left eye, strabismus, high-arched palate, malocclusion, severe kyphoscoliosis, bilateral calcaneovalgus fo…

0301 basic medicinePathologymedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesGenotype-phenotype correlationNeurofibromatosesLisch noduleContiguous gene syndromePopulationCase ReportContiguous gene syndromeChromosomesCraniofacial Abnormalities03 medical and health sciences0302 clinical medicineAtypical deletionIntellectual DisabilitymedicineHumansMultiplex ligation-dependent probe amplificationNeurofibromatosiseducationChildPreschoolNeurofibromatoseseducation.field_of_studybusiness.industryLearning DisabilitiesPair 17lcsh:RJ1-570Axillary frecklinglcsh:Pediatricsmedicine.diseaseeye diseasesMLPA030104 developmental biologyNF1 geneChild PreschoolFemalemedicine.symptomChromosome DeletionbusinessAtypical deletion; Contiguous gene syndrome; Genotype-phenotype correlation; MLPA; NF1 gene; Child Preschool; Chromosome Deletion; Chromosomes Human Pair 17; Craniofacial Abnormalities; Female; Humans; Intellectual Disability; Learning Disabilities; Neurofibromatoses030217 neurology & neurosurgeryChromosomes Human Pair 17Comparative genomic hybridizationHumanItalian Journal of Pediatrics
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KnotGenome: a server to analyze entanglements of chromosomes.

2018

Abstract The KnotGenome server enables the topological analysis of chromosome model data using three-dimensional coordinate files of chromosomes as input. In particular, it detects prime and composite knots in single chromosomes, and links between chromosomes. The knotting complexity of the chromosome is presented in the form of a matrix diagram that reveals the knot type of the entire polynucleotide chain and of each of its subchains. Links are determined by means of the Gaussian linking integral and the HOMFLY-PT polynomial. Entangled chromosomes are presented graphically in an intuitive way. It is also possible to relax structure with short molecular dynamics runs before the analysis. Kn…

0301 basic medicinePolynomialProtein ConformationGaussianPolynucleotidesBiologyType (model theory)Molecular Dynamics SimulationPrime (order theory)ChromosomesQuantitative Biology::Subcellular Processes03 medical and health sciencessymbols.namesakeMatrix (mathematics)Knot (unit)Chain (algebraic topology)GeneticsDiscrete mathematicsInternetDiagramComputational BiologyMathematics::Geometric TopologyQuantitative Biology::Genomics030104 developmental biologyWeb Server IssuesymbolsAlgorithmsSoftwareNucleic acids research
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Analysis of Plasminogen Genetic Variants in Multiple Sclerosis Patients.

2016

Multiple sclerosis (MS) is a prevalent neurological disease of complex etiology. Here, we describe the characterization of a multi-incident MS family that nominated a rare missense variant (p.G420D) in plasminogen (PLG) as a putative genetic risk factor for MS. Genotyping of PLG p.G420D (rs139071351) in 2160 MS patients, and 886 controls from Canada, identified 10 additional probands, two sporadic patients and one control with the variant. Segregation in families harboring the rs139071351 variant, identified p.G420D in 26 out of 30 family members diagnosed with MS, 14 unaffected parents, and 12 out of 30 family members not diagnosed with disease. Despite considerably reduced penetrance, lin…

0301 basic medicineProbandMaleGene ExpressionQH426-470multiple sclerosis0302 clinical medicineRisk FactorsGenotypeMissense mutationExomegeneticsguidelinesGenetics (clinical)degradationriskGeneticsLinkagedeficiencyMiddle AgedPenetrance3. Good healthPedigreeplasminogenChromosomes Human Pair 6FemalelinkageAdultGenotype610 Medicine & healthInvestigationsBiologysystemPolymorphism Single Nucleotideblood-brain-barrieractivatorMultiple sclerosisAssociation03 medical and health scienceslamininGenetic linkagemedicineGeneticsHumansAmino Acid Sequenceddc:610Molecular BiologyGenotypingAgeddiseaseSequence Homology Amino AcidMultiple sclerosisCase-control studyassociationPlasminogenmedicine.diseasediagnostic-criteria030104 developmental biologyCase-Control StudiesImmunologySequence Alignment030217 neurology & neurosurgery
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7q31.32 partial duplication: First report of a child with dysmorphism, autistic spectrum disorder, moderate intellectual disability and, epilepsy. Li…

2019

Abstract Introduction Duplication of long arm of chromosome 7(q) is uncommon. It may occur as “pure”, isolated anomaly or in association with other mutations involving the same or other chromosomes. “Pure” chromosome 7q duplication has recently been classified by segment involved: the interstitial, proximal, or distal segment of the arm. Attempts to correlate genotype with phenotype in each group has yielded questionable results even though intellective disability and minor dysmorphic features of variable types are typically seen. Material and Methods In a young boy showing minor facial dysmorphism, language delay, autistic spectrum disorder, epileptic seizures, behavioral disturbances and …

0301 basic medicineProbandPediatricsmedicine.medical_specialtyAutism Spectrum DisorderLanguage delayDevelopmental DisabilitiesIrritabilityChromosomes03 medical and health sciencesEpilepsy0302 clinical medicineIntellectual DisabilityGene duplicationIntellectual disabilityHumansMedicineGenetic Association StudiesChromosome 7 (human)Epilepsybusiness.industrymedicine.disease7q31.32 duplicationDysmorphism030104 developmental biologyAutistic spectrum disorderNeurologyAutism spectrum disorderPair 7Neurology (clinical)medicine.symptombusinessChromosomes Human Pair 7030217 neurology & neurosurgeryHumanEpilepsy Research
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SPEN haploinsufficiency causes a neurodevelopmental disorder overlapping proximal 1p36 deletion syndrome with an episignature of X chromosomes in fem…

2021

Contains fulltext : 231702.pdf (Publisher’s version ) (Closed access) Deletion 1p36 (del1p36) syndrome is the most common human disorder resulting from a terminal autosomal deletion. This condition is molecularly and clinically heterogeneous. Deletions involving two non-overlapping regions, known as the distal (telomeric) and proximal (centromeric) critical regions, are sufficient to cause the majority of the recurrent clinical features, although with different facial features and dysmorphisms. SPEN encodes a transcriptional repressor commonly deleted in proximal del1p36 syndrome and is located centromeric to the proximal 1p36 critical region. Here, we used clinical data from 34 individuals…

0301 basic medicineSHARPMaleobesitygenotype-phenotype correlationsAutism Spectrum DisorderPROTEINChromosome DisordersHaploinsufficiencyRNA-Binding ProteinPHENOTYPE CORRELATIONS1p36; distal 1p36 deletion syndrome; DNA methylome analysis; episignature; genotype-phenotype correlations; neurodevelopmental disorder; obesity; proximal 1p36 deletion syndrome; SPEN; X chromosome; Adolescent; Autism Spectrum Disorder; Child; Child Preschool; Chromosome Deletion; Chromosome Disorders; Chromosomes Human Pair 1; Chromosomes Human X; DNA Methylation; DNA-Binding Proteins; Epigenesis Genetic; Female; Haploinsufficiency; Humans; Intellectual Disability; Male; Neurodevelopmental Disorders; Phenotype; RNA-Binding Proteins; Young AdultEpigenesis GeneticX chromosome0302 clinical medicineNeurodevelopmental disorderNeurodevelopmental DisorderIntellectual disabilityMOLECULAR CHARACTERIZATIONdistal 1p36 deletion syndromeChildGenetics (clinical)X chromosomeGeneticsXDNA methylome analysiRNA-Binding ProteinsSPLIT-ENDSHypotoniaDNA-Binding ProteinsPhenotypeAutism spectrum disorderChromosomes Human Pair 1Child PreschoolDNA methylome analysisMONOSOMY 1P36Pair 1SPENFemalemedicine.symptomChromosome DeletionHaploinsufficiencyRare cancers Radboud Institute for Health Sciences [Radboudumc 9]HumanAdolescentDNA-Binding ProteinBiologygenotype-phenotype correlationChromosomes03 medical and health sciencesYoung AdultGeneticSDG 3 - Good Health and Well-beingReportIntellectual DisabilityREVEALSGeneticsmedicineHumansEpigeneticsPreschoolChromosomes Human XNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]1p361p36 deletion syndromeIDENTIFICATIONMUTATIONSproximal 1p36 deletion syndromeDNA Methylationmedicine.diseaseneurodevelopmental disorderGENEepisignature030104 developmental biologyChromosome DisorderNeurodevelopmental Disorders030217 neurology & neurosurgeryEpigenesis
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P/CAF-mediated spermidine acetylation regulates histone acetyltransferase activity

2016

Histones and polyamines are important determinants of the chromatin structure. Histones form the core of nucleosome particles and their modification by acetylation of N-terminal tails is involved in chromatin structural changes and transcriptional regulation. Polyamines, including spermidine, are also targets of both cytoplasmic and nuclear acetylation, which in turn alters their affinity for DNA and nucleosomes. Previous studies report the interplay between polyamines metabolism and levels of histone acetylation, but the molecular basis of this effect is still unclear. In this work, we have analyzed the in vitro effect of spermidine on histone H3 acetylation catalyzed by P/CAF, a highly co…

0301 basic medicineSpermidine acetylationSpermidineSAP30BiologyHistones03 medical and health sciences0302 clinical medicineHistone H1Drug DiscoveryHistone H2AAnimalsHistone acetyltransferase activityp300-CBP Transcription FactorsHistone octamerHistone H3 acetylationHistone AcetyltransferasesPolytene ChromosomesPharmacologyAcetylationGeneral MedicineHistone acetyltransferaseEnzyme ActivationKineticsDrosophila melanogaster030104 developmental biologyBiochemistry030220 oncology & carcinogenesisbiology.proteinJournal of Enzyme Inhibition and Medicinal Chemistry
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Simulation-based estimation of branching models for LTR retrotransposons

2017

Abstract Motivation LTR retrotransposons are mobile elements that are able, like retroviruses, to copy and move inside eukaryotic genomes. In the present work, we propose a branching model for studying the propagation of LTR retrotransposons in these genomes. This model allows us to take into account both the positions and the degradation level of LTR retrotransposons copies. In our model, the duplication rate is also allowed to vary with the degradation level. Results Various functions have been implemented in order to simulate their spread and visualization tools are proposed. Based on these simulation tools, we have developed a first method to evaluate the parameters of this propagation …

0301 basic medicineStatistics and ProbabilitySource codeTheoretical computer scienceRetroelementsmedia_common.quotation_subjectRetrotransposon[INFO.INFO-SE]Computer Science [cs]/Software Engineering [cs.SE]BiologyBiochemistryGenomeChromosomesBranching (linguistics)[INFO.INFO-IU]Computer Science [cs]/Ubiquitous Computing03 medical and health sciences[INFO.INFO-CR]Computer Science [cs]/Cryptography and Security [cs.CR]SoftwareAnimalsComputer SimulationMolecular BiologyComputingMilieux_MISCELLANEOUSmedia_commoncomputer.programming_languageGeneticsGenomeModels Geneticbusiness.industry[SDV.BID.EVO]Life Sciences [q-bio]/Biodiversity/Populations and Evolution [q-bio.PE]Python (programming language)[SDV.BIBS]Life Sciences [q-bio]/Quantitative Methods [q-bio.QM][INFO.INFO-MO]Computer Science [cs]/Modeling and SimulationComputer Science ApplicationsVisualizationComputational Mathematics030104 developmental biologyDrosophila melanogasterComputational Theory and Mathematics[INFO.INFO-MA]Computer Science [cs]/Multiagent Systems [cs.MA]Programming Languages[INFO.INFO-ET]Computer Science [cs]/Emerging Technologies [cs.ET]Mobile genetic elements[INFO.INFO-DC]Computer Science [cs]/Distributed Parallel and Cluster Computing [cs.DC]businesscomputerSoftware
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The Coat-Hanger Angle Sign

2016

An infant boy, the second child of healthy parents, was born at 35.5 weeks of gestation by cesarean delivery performed in emergency because of fetal bradycardia and polyhydramnios. At birth his weight was 2770 g (62nd percentile), length 48.3 cm (69th percentile), and head circumference 33.5 cm (64th percentile). Findings of a phys- ical examination showed a broad forehead, a depressed nasal bridge, anteverted nares, a long and protruding philtrum, a high arched palate, retrognathia, joint contractures, and an umbilical hernia. The Apgar score was 6/8 at 1/5 minutes. Because of progressive respiratory distress he required hos- pitalization and noninvasive support ventilation for the first 3…

0301 basic medicineThoraxMaleCoatPediatricsmedicine.medical_specialtyUpd(14)pat030105 genetics & heredityCHA; Kagami-Ogata syndrome; Upd(14)pat; Pediatrics Perinatology and Child HealthKAGAMI-OGATA SYNDROME03 medical and health sciencesmedicineHumansAbnormalities MultipleChromosomes Human Pair 14business.industryKagami-Ogata syndromeInfant NewbornInfantAnatomyThoraxUniparental Disomymedicine.diseaseInfant newbornUniparental disomyPediatrics Perinatology and Child HealthCHAbusinessSign (mathematics)
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11q Deletion or ALK Activity Curbs DLG2 Expression to Maintain an Undifferentiated State in Neuroblastoma

2020

High-risk 11q deleted neuroblastomas typically display undifferentiated/poorly differentiated morphology. Neuroblastoma is thought to develop from Schwann cell precursors and undifferentiated neural crest (NC) derived cells. It is therefore vital to understand mechanisms involved in the block of differentiation. We identify an important role for oncogenic ALK-ERK1/2-SP1 signaling in maintenance of undifferentiated NC-derived progenitors via repression of DLG2, a tumor suppressor in neuroblastoma. DLG2 is expressed in the ‘bridge signature’ that represents the transcriptional transition state when neural crest cells or Schwann Cell Precursors become chromaffin cells of the adrenal gland. We …

0301 basic medicineTranscription GeneticCarcinogenesisChromaffin CellsRetinoic acidlaw.inventionNeuroblastomachemistry.chemical_compound0302 clinical medicinelawNerve Growth FactorMedicine and Health Sciencesretinoic acidAnaplastic Lymphoma Kinaselcsh:QH301-705.5NeuronsMice Inbred BALB CNeural crestCell DifferentiationPrognosisCandidate Tumor Suppressor GeneDLG2Up-RegulationCell biologyGene Expression Regulation NeoplasticERKPhenotypeTreatment Outcomemedicine.anatomical_structureFemaleChromosome Deletiontumor suppressorMAP Kinase Signaling SystemSp1 Transcription FactorSchwann cellGenetics and Molecular BiologyTretinoinBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAdrenergic AgentsCell Line TumorNeuroblastomamedicineAnimalsHumansProgenitor cellGenePsychological repressionCell ProliferationChromosomes Human Pair 11Tumor Suppressor Proteinsmedicine.disease030104 developmental biologyALKlcsh:Biology (General)chemistryTrk receptorGeneral BiochemistrySuppressorSchwann CellsGuanylate Kinases030217 neurology & neurosurgerySSRN Electronic Journal
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Susceptibility to Heart Defects in Down Syndrome Is Associated with Single Nucleotide Polymorphisms in HAS 21 Interferon Receptor Cluster and VEGFA G…

2020

Background: Congenital heart defects (CHDs) are present in about 40&ndash

0301 basic medicineVEGFAAdultHeart Defects CongenitalMaleVascular Endothelial Growth Factor ADown syndromelcsh:QH426-470AdolescentChromosomes Human Pair 21Down syndromeSNPSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideArticle03 medical and health sciencesHeart disorder0302 clinical medicineGenotypeGeneticsmedicineHumansGeneGenetics (clinical)IFNRReceptors InterferonGeneticsmedicine.diseasePhenotypeHeart defectlcsh:GeneticsVascular endothelial growth factor A030104 developmental biologySettore MED/03 - Genetica Medica030220 oncology & carcinogenesisMultigene Familyheart defectsFemaleChromosome 21SNPsGenes
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