Search results for "genetic diseases"

showing 10 items of 56 documents

Laboratory investigations in genetic syndromes: examples of clinical approach in the neonatal unit.

2010

Contiguous gene deletion syndromes: the importance of an accurate genetic definition for a careful clinical monitoring. Contiguous gene deletion syndromes are so named because the deletion manifests as a distinctive cluster of otherwise unrelated single-gene disorders in the same subject. An accurate genetic definition of the deleted region is extremely important for the appropriate management of these patients and for unravelling the function of the involved genes. The microarray-based comparative genomic hybridization (CGH arrays) analysis is the actual molecular method able to accurately define the bounds of a deleted region, since it allows an evaluation of DNA copy number alterations a…

MaleComparative Genomic Hybridizationgenetic syndrome neonategenetic syndromesDisorders of Sex DevelopmentGene DosageGenetic Diseases InbornInfant NewbornLaboratories HospitalEarly DiagnosisPhenotypeSettore MED/38 - Pediatria Generale E SpecialisticaIntensive Care Units NeonatalIntensive Care NeonatalChromosomes HumanHumansFemaleGenetic TestingGene Deletion
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X-linked primary ciliary dyskinesia due to mutations in the cytoplasmic axonemal dynein assembly factor PIH1D3

2017

By moving essential body fluids and molecules, motile cilia and flagella govern respiratory mucociliary clearance, laterality determination and the transport of gametes and cerebrospinal fluid. Primary ciliary dyskinesia (PCD) is an autosomal recessive disorder frequently caused by non-assembly of dynein arm motors into cilia and flagella axonemes. Before their import into cilia and flagella, multi-subunit axonemal dynein arms are thought to be stabilized and pre-assembled in the cytoplasm through a DNAAF2–DNAAF4–HSP90 complex akin to the HSP90 co-chaperone R2TP complex. Here, we demonstrate that large genomic deletions as well as point mutations involving PIH1D3 are responsible for an X-li…

MaleCytoplasmProtein FoldingAxoneme[SDV]Life Sciences [q-bio][SDV.GEN] Life Sciences [q-bio]/Genetics[SDV.MHEP.PSR]Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractouterGenes X-LinkedChilddefectsPhylogenyZebrafisharmsSequence DeletionvariantsIntracellular Signaling Peptides and ProteinsGenetic Diseases X-LinkedPedigreeMultidisciplinary Sciences[SDV] Life Sciences [q-bio]motilityChild PreschoolMicrotubule ProteinsSperm MotilityScience & Technology - Other TopicsFemaleAdultAdolescentinnerUK10K Rare Groupr2tp complexof-function mutationsArticleMicroscopy Electron TransmissionMD MultidisciplinaryExome SequencingAnimalsHumansPoint MutationCiliaHSP90 Heat-Shock Proteins[SDV.GEN]Life Sciences [q-bio]/GeneticsScience & TechnologyKartagener SyndromeInfant NewbornAxonemal DyneinsDisease Models AnimalHEK293 Cells[SDV.MHEP.PSR] Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractidentifies mutationsproteinApoptosis Regulatory ProteinsSequence AlignmentMolecular ChaperonesNature Communications
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Next-generation sequencing confirms the implication of SLC24A1 in autosomal-recessive congenital stationary night blindness.

2015

Congenital stationary night blindness (CSNB) is a clinically and genetically heterogeneous retinal disorder which represents rod photoreceptor dysfunction or signal transmission defect from photoreceptors to adjacent bipolar cells. Patients displaying photoreceptor dysfunction show a Riggs-electroretinogram (ERG) while patients with a signal transmission defect show a Schubert-Bornschein ERG. The latter group is subdivided into complete or incomplete (ic) CSNB. Only few CSNB cases with Riggs-ERG and only one family with a disease-causing variant in SLC24A1 have been reported. Whole-exome sequencing (WES) in a previously diagnosed icCSNB patient identified a homozygous nonsense variant in SL…

MaleGenes RecessiveSodium-Calcium ExchangerNight BlindnessElectroretinographyMyopiaHumansExomeGenetic Predisposition to DiseaseAmino Acid SequenceSLC24A1Family HealthHigh-throughput sequencingBase SequenceSequence Homology Amino AcidSettore MED/30 - Malattie Apparato VisivoHomozygoteHigh-Throughput Nucleotide SequencingEye Diseases HereditaryGenetic Diseases X-LinkedPedigreeNight BlindneMutationFemaleCongenital stationary night blindneHumanClinical genetics
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Noninvasive assessment of respiratory muscle strength and activity in Myotonic dystrophy

2017

Objective To evaluate sensitivity/specificity of the maximum relaxation rate (MRR) of inspiratory muscles, amplitude of electromyographic activity of the sternocleidomastoid (SCM), scalene (SCA), parasternal (2ndIS) and rectus abdominis (RA) muscles; lung function and respiratory muscle strength in subjects with Myotonic dystrophy type 1 (DM1) compared with healthy subjects. Design and methods Quasi-experimental observational study with control group. MRR of inspiratory muscles, lung function and amplitude of the electromyographic activity of SCM, SCA, 2ndIS and RA muscles during maximum inspiratory pressure (PImax), maximum expiratory pressure (PEmax) and sniff nasal inspiratory pressure (…

MaleMuscle PhysiologyTime FactorsMuscle FunctionsPhysiologyMuscle RelaxationRespiratory Systemlcsh:MedicineElectromyographyPulmonary function testing0302 clinical medicineThoracic DiaphragmMedicine and Health SciencesMyotonic DystrophyMedicineRespiratory systemlcsh:ScienceMusculoskeletal SystemAbdominal MusclesMultidisciplinaryAnthropometrymedicine.diagnostic_testMusclesMuscle AnalysisRespiratory MusclesRespiratory Function TestsBioassays and Physiological AnalysisMuscle relaxationInhalationGenetic DiseasesExhalationParasternal lineCardiologyFemaleAnatomyMuscle ElectrophysiologyResearch ArticleAdult; Anthropometry; Electromyography; Exhalation; Female; Humans; Inhalation; Male; Muscle Relaxation; Muscle Strength; Myotonic Dystrophy; Pressure; ROC Curve; Respiratory Function Tests; Respiratory Muscles; Sample Size; Time FactorsAdultmedicine.medical_specialtyRespiratory physiologyResearch and Analysis Methods03 medical and health sciencesInternal medicineRespiratory musclesPressureRespiratory muscleHumansRespiratory PhysiologyMuscle StrengthClinical GeneticsElectromyographic activityElectromyographybusiness.industryElectrophysiological Techniqueslcsh:RBiology and Life SciencesExhalationSkeletal MusclesROC Curve030228 respiratory systemSample Sizelcsh:Qbusiness030217 neurology & neurosurgeryPLOS ONE
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Further delineation of eye manifestations in homozygous 15q13.3 microdeletions including TRPM1: a differential diagnosis of ceroid lipofuscinosis.

2014

The 15q13.3 heterozygous microdeletion is a fairly common microdeletion syndrome with marked clinical variability and incomplete penetrance. The average size of the deletion, which comprises six genes including CHRNA7, is 1.5 Mb. CHRNA7 has been identified as the gene responsible for the neurological phenotype in this microdeletion syndrome. Only seven patients with a homozygous microdeletion that includes at least CHRNA7, and is inherited from both parents have been described in the literature. The aim of this study was to further describe the distinctive eye manifestations from the analysis in the three French patients diagnosed with the classical 1.5 Mb homozygous microdeletion. Patients…

MalePathologymedicine.medical_specialtygenetic structuresalpha7 Nicotinic Acetylcholine ReceptorEncephalopathyTRPM Cation ChannelsChromosome DisordersBiologyBlindnessEyePupilNeuronal Ceroid-LipofuscinosesNight BlindnessSeizuresIntellectual DisabilityRetinal DystrophiesGeneticsmedicineElectroretinographyMyopiaHumansEye AbnormalitiesChildGenetics (clinical)TRPM1Genetic Association StudiesCongenital stationary night blindnessGeneticsChromosomes Human Pair 15DystrophyEye Diseases HereditaryGenetic Diseases X-LinkedOptic NerveMicrodeletion syndromemedicine.diseasePenetranceChild PreschoolFemalesense organsDifferential diagnosisChromosome DeletionAmerican journal of medical genetics. Part A
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"I Know that You Know that I Know": Neural Substrates Associated with Social Cognition Deficits in DM1 Patients.

2016

Myotonic dystrophy type-1 (DM1) is a genetic multi-systemic disorder involving several organs including the brain. Despite the heterogeneity of this condition, some patients with non-congenital DM1 can present with minimal cognitive impairment on formal testing but with severe difficulties in daily-living activities including social interactions. One explanation for this paradoxical mismatch can be found in patients' dysfunctional social cognition, which can be assessed in the framework of the Theory of Mind (ToM). We hypothesize here that specific disease driven abnormalities in DM1 brains may result in ToM impairments. We recruited 20 DM1 patients who underwent the "Reading the Mind in th…

MaleSocial CognitionMagnetic Resonance SpectroscopyTheory of MindAdult; Brain; Cognition; Female; Humans; Magnetic Resonance Spectroscopy; Male; Middle Aged; Myotonic Dystrophy; Neuropsychological Tests; Social Behavior; Theory of MindSocial Scienceslcsh:MedicineDiseaseNeuropsychological TestsDiagnostic RadiologyCognition0302 clinical medicineFunctional Magnetic Resonance ImagingTheory of mindMedicine and Health SciencesPsychologyMyotonic Dystrophylcsh:ScienceCognitive ImpairmentBrain MappingMultidisciplinarymedicine.diagnostic_testCognitive NeurologyRadiology and Imagingagricultural and biological sciences (all); biochemistry genetics and molecular biology (all); medicine (all)05 social sciencesRBrainCognitionMiddle AgedMagnetic Resonance ImagingNeurologyRC0346Genetic DiseasesPhysical SciencesFemaleSettore MED/26 - NeurologiaPsychologyResearch ArticleClinical psychologyAdultmusculoskeletal diseasesComputer and Information Sciencesmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesSocial PsychologyImaging TechniquesCognitive NeuroscienceNeuroimagingDysfunctional familyResearch and Analysis MethodsMyotonic dystrophy050105 experimental psychology03 medical and health sciencesDiagnostic MedicineSocial cognitionTheory of mind cerebral lesionGeneticsmedicineHumans0501 psychology and cognitive sciencesSocial BehaviorPsychiatryClinical GeneticsSettore M-PSI/02 - Psicobiologia E Psicologia Fisiologicalcsh:RCognitive PsychologyBiology and Life SciencesHuman Geneticsmedicine.diseaseComprehensionGraph TheoryRC0321Cognitive Sciencelcsh:QFunctional magnetic resonance imagingMathematics030217 neurology & neurosurgeryNeurosciencePLoS ONE
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Results of mitral valve repair for Barlow disease (bileaflet prolapse) via right minithoracotomy versus conventional median sternotomy: a randomized …

2011

Objective: The results of mitral repair for complex Barlow valves are adequate and support earlier intervention. It is unknown whether these results are reproducible in the context of minimally invasive surgery via right minithoracotomy. Methods: We randomized patients with Barlow mitral disease (bileaflet prolapse) to have conventional open repair via median sternotomy (MS group) or minimally invasive (MI group) repair. Repair was done using polytetrafluoroethylene chordal reimplantation for both leaflets. In the MI group, we adopted right minithoracotomy, peripheral cannulation, external aortic clamping, and surgery under direct vision. Results: Both groups comprised 70 patients. The oper…

MaleTime Factorsmedicine.medical_treatmentKaplan-Meier Estimatelaw.inventionlawRisk FactorsMitral valveCardiac Surgical ProcedureHospital MortalityProspective StudiesUltrasonographyPain PostoperativeMitral Valve ProlapseAtrial fibrillationGenetic Diseases X-LinkedMiddle Agedmedicine.anatomical_structureTreatment OutcomeItalyThoracotomyCardiologyMitral ValveFemaleCardiology and Cardiovascular MedicineHumanPulmonary and Respiratory MedicineAdultReoperationmedicine.medical_specialtyTime FactorContext (language use)Risk AssessmentInternal medicineCardiopulmonary bypassmedicineHumansCardiac Surgical ProceduresMechanical ventilationMitral valve repairMitral regurgitationChi-Square Distributionbusiness.industryRisk FactorPatient SelectionSettore MED/23 - Chirurgia Cardiacamedicine.diseaseSternotomySurgeryProspective StudieMedian sternotomySurgerybusinessThe Journal of thoracic and cardiovascular surgery
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Mild phenotypes in a series of patients with Opitz GBBB syndrome with MID1 mutations

2004

Contains fulltext : 48815.pdf (Publisher’s version ) (Closed access) Opitz syndrome (OS; MIM 145410 and MIM 300000) is a congenital midline malformation syndrome characterized by hypertelorism, hypospadias, cleft lip/palate, laryngotracheoesophageal (LTE) abnormalities, imperforate anus, developmental delay, and cardiac defects. The X-linked form (XLOS) is caused by mutations in the MID1 gene, which encodes a microtubule-associated RBCC protein. In this study, phenotypic manifestations of patients with and without MID1 mutations were compared to determine genotype-phenotype correlations. We detected 10 novel mutations, 5 in familial cases, 2 in sporadic cases, and 3 in families for whom it …

Malemedicine.medical_specialtyUbiquitin-Protein LigasesBiologymedicine.disease_causeGastroenterologyG/BBB SYNDROMEFAMILIESGenomic disorders and inherited multi-system disorders [IGMD 3]Genotype-phenotype distinctionInternal medicineGeneticsmedicineHumansHypertelorismGeneGenetics (clinical)GeneticsFamily HealthX-linked Opitz syndromeMutationMID1Nuclear ProteinsGenetic Diseases X-LinkedExonsOpitz G/BBB Syndromemedicine.diseasePhenotypeGENEPedigreeSmith-Lemli-Opitz SyndromePhenotypeGenetic defects of metabolism [UMCN 5.1]HypospadiasMutationMicrotubule ProteinsFemalephenotypic variabilityXP22medicine.symptomImperforate anusFunctional Neurogenomics [DCN 2]BBBTranscription FactorsAmerican Journal of Medical Genetics. Part A
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Three-Year Results of Repaired Barlow Mitral Valves via Right Minithoracotomy versus Median Sternotomy in a Randomized Trial

2012

<b><i>Objectives:</i></b> To clarify whether the results of repair of a complex mitral lesion (Barlow valve) at the intermediate-term follow-up are independent of the mode of surgical access [minithoracotomy vs. median sternotomy (MS)]. <b><i>Methods:</i></b> In a prospective randomized study of mitral repair for Barlow disease using either a minimally invasive (MI) approach or MS, we achieved an average follow-up of 3 years (echocardiography, physical examination and quality of life). Mitral repair was achieved with polytetrafluoroethylene chordal implantation for both leaflets. <b><i>Results:</i></b> Both groups inclu…

Malemedicine.medical_specialtymedicine.medical_treatmentFollow-Up Studielaw.inventionLesionRandomized controlled trialMinimally invasive surgerylawmedicineHumansMitral Valve StenosisPharmacology (medical)Prospective StudiesMitral Valve Stenosicardiovascular diseasesMitral valve repairMitral Valve Prolapsebusiness.industryFollow-upMedicine (all)Mitral Valve InsufficiencyGenetic Diseases X-LinkedMiddle AgedSternotomySurgeryProspective StudieTreatment OutcomeThoracotomyMedian sternotomyQuality of Lifecardiovascular systemMitral ValveFemalemedicine.symptomCardiology and Cardiovascular MedicinebusinessMitral valve repairFollow-Up StudiesHumanCardiology
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Proteomic identification of FHL1 as the protein mutated in human reducing body myopathy

2007

Reducing body myopathy (RBM) is a rare disorder causing progressive muscular weakness characterized by aggresome-like inclusions in the myofibrils. Identification of genes responsible for RBM by traditional genetic approaches has been impossible due to the frequently sporadic occurrence in affected patients and small family sizes. As an alternative approach to gene identification, we used laser microdissection of intracytoplasmic inclusions identified in patient muscle biopsies, followed by nanoflow liquid chromatography-tandem mass spectrometry and proteomic analysis. The most prominent component of the inclusions was the Xq26.3-encoded four and a half LIM domain 1 (FHL1) protein, expresse…

Models MolecularProteomicsMolecular Sequence DataMuscle ProteinsBiologyTransfectionProteomicsInclusion bodiesMuscular DiseasesmedicineAmino Acid SequenceLaser capture microdissectionInclusion BodiesIntracellular Signaling Peptides and ProteinsCardiac muscleSkeletal muscleGenetic Diseases X-LinkedGeneral MedicineLIM Domain Proteinsmedicine.diseaseCongenital myopathyMolecular biologyFHL1medicine.anatomical_structureMutationMyofibrilResearch Article
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