Search results for "BAND"

showing 10 items of 2610 documents

A systematic variant screening in familial cases of congenital heart defects demonstrates the usefulness of molecular genetics in this field

2016

International audience; The etiology of congenital heart defect (CHD) combines environmental and genetic factors. So far, there were studies reporting on the screening of a single gene on unselected CHD or on familial cases selected for specific CHD types. Our goal was to systematically screen a proband of familial cases of CHD on a set of genetic tests to evaluate the prevalence of disease-causing variant identification. A systematic screening of GATA4, NKX2-5, ZIC3 and Multiplex ligation-dependent probe amplification (MLPA) P311 Kit was setup on the proband of 154 families with at least two cases of non-syndromic CHD. Additionally, ELN screening was performed on families with supravalvula…

0301 basic medicineProbandMaleCardiomyopathy22q11.2Disease030204 cardiovascular system & hematologyBioinformatics0302 clinical medicinede-novoEpidemiology3 large registriesGenetics (clinical)zic3 mutationsGeneticsHigh-Throughput Nucleotide Sequencing3. Good healthPedigreeHomeobox Protein Nkx-2.5malformationsFemaleepidemiologyHeart Defects Congenitalmedicine.medical_specialtyGenetic counselingArticle03 medical and health sciences[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyMolecular geneticsGeneticsmedicineHumansMultiplex ligation-dependent probe amplificationGenetic TestingHomeodomain Proteinsdiseasebusiness.industryvariabilityGenetic Variationmedicine.diseaseGATA4 Transcription Factor030104 developmental biologyMutationEtiologycardiovascular defectsbusinessMultiplex Polymerase Chain Reactioncardiomyopathy[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyTranscription Factors
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Mutations in the GLA Gene and LysoGb3: Is It Really Anderson-Fabry Disease?

2018

Anderson-Fabry disease (FD) is a rare, progressive, multisystem storage disorder caused by the partial or total deficit of the lysosomal enzyme &alpha

0301 basic medicineProbandMaleDiseasemedicine.disease_causeSphingolipidCatalysilcsh:Chemistry0302 clinical medicineGla geneFabry disease; GLA gene; LysoGb3MedicineChildlcsh:QH301-705.5Spectroscopychemistry.chemical_classificationGeneticsAlleleAged 80 and overMutationComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineMiddle AgedPhenotype3. Good healthComputer Science ApplicationsPhenotypeChild PreschoolFemaleHumanAdultAdolescentGenotypeGlycolipidCatalysisArticleInorganic Chemistry03 medical and health sciencesYoung Adultotorhinolaryngologic diseasesHumansPhysical and Theoretical ChemistryMolecular BiologyGeneGLA geneAllelesAgedFabry diseaseSphingolipidsbusiness.industryOrganic ChemistryInfant NewbornLysoGb3InfantBiomarkerFabry disease; gla gene; lysogb3; adolescent; adult; aged; aged 80 and over; alleles; amino acid substitution; biomarkers; child; child preschool; fabry disease; female; genotype; glycolipids; humans; infant; infant newborn; male; middle aged; phenotype; sphingolipids; young adult; alpha-galactosidase; mutationmedicine.diseaseFabry disease030104 developmental biologyEnzymechemistrylcsh:Biology (General)lcsh:QD1-999Amino Acid Substitutionalpha-GalactosidaseMutationGlycolipidsbusiness030217 neurology & neurosurgeryBiomarkersInternational Journal of Molecular Sciences
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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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HCN1 mutation spectrum: from neonatal epileptic encephalopathy to benign generalized epilepsy and beyond

2018

International audience; Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels control neuronal excitability and their dysfunction has been linked to epileptogenesis but few individuals with neurological disorders related to variants altering HCN channels have been reported so far. In 2014, we described five individuals with epileptic encephalopathy due to de novo HCN1 variants. To delineate HCN1-related disorders and investigate genotype-phenotype correlations further, we assembled a cohort of 33 unpublished patients with novel pathogenic or likely pathogenic variants: 19 probands carrying 14 different de novo mutations and four families with dominantly inherited variants segre…

0301 basic medicineProbandMaleModels MolecularPotassium Channels[SDV]Life Sciences [q-bio]Medizinmedicine.disease_causeEpileptogenesisMembrane PotentialsEpilepsy0302 clinical medicineHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsMissense mutationChildGeneticsMutationMiddle AgedPhenotype3. Good healthTransmembrane domainclinical spectrum; epilepsy; HCN1; intellectual disability; ion channelintellectual disabilityChild PreschoolEpilepsy GeneralizedFemaleSpasms InfantileAdultAdolescentCHO CellsBiology03 medical and health sciencesYoung AdultCricetulusHCN1medicineAnimalsHumansGeneralized epilepsyGenetic Association StudiesAgedInfantmedicine.diseaseElectric Stimulationclinical spectrum030104 developmental biologyMutationion channelMutagenesis Site-DirectedepilepsyNeurology (clinical)030217 neurology & neurosurgery
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Familial Central Hypothyroidism Caused by a Novel IGSF1 Gene Mutation.

2016

Congenital hypothyroidism of central origin (CH-C) is a rare disease in which thyroid hormone deficiency is caused by insufficient thyrotropin stimulation of a normal thyroid gland. A recently described syndrome of isolated CH-C and macroorchidism was attributed to loss-of-function mutations of the immunoglobulin superfamily, member 1 gene (IGSF1).CH-C was diagnosed in three siblings. The TRH, TRHR, and TSHB genes were sequenced followed by whole-exome sequencing in the proband. A mutation identified in IGSF1 was analyzed by direct PCR sequencing in family members. The effects of the mutation were assessed by in vitro studies in HEK293 cells.The index case was negative for mutations in TRH,…

0301 basic medicineProbandMaleendocrine systemEndocrinology Diabetes and MetabolismDNA Mutational AnalysisImmunoglobulinsThyrotropin030209 endocrinology & metabolismBiology03 medical and health sciences0302 clinical medicineEndocrinologyHypothyroidismmedicineCentral hypothyroidismCongenital HypothyroidismHumansInsertionThyrotropin-Releasing HormoneGeneticsMacroorchidismReceptors Thyrotropin-Releasing HormoneSiblingsThyroidInfant NewbornInfantMembrane Proteinsmedicine.diseaseMolecular biologyCongenital hypothyroidismIGSF1030104 developmental biologymedicine.anatomical_structureHEK293 CellsChild PreschoolMutation (genetic algorithm)MutationThyroid : official journal of the American Thyroid Association
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Confirmation of PDZD7 as a Nonsyndromic Hearing Loss Gene.

2016

Objective PDZD7 was identified in 2009 in a family with apparent nonsyndromic sensorineural hearing loss. However, subsequent clinical reports have associated PDZD7 with digenic Usher syndrome, the most common cause of deaf-blindness, or as a modifier of retinal disease. No further reports have validated this gene for nonsyndromic hearing loss, intuitively calling correct genotype-phenotype association into question. This report describes a validating second case for biallelic mutations in PDZD7 causing nonsyndromic mild to severe sensorineural hearing loss. It also provides detailed audiometric and ophthalmologic data excluding Usher syndrome in both the present proband (proband 1) and the…

0301 basic medicineProbandMalemedicine.medical_specialtyHeterozygoteAdolescentHearing lossUsher syndromeHearing Loss SensorineuralOtoacoustic Emissions SpontaneousAudiologyCompound heterozygosity03 medical and health sciencesSpeech and Hearing0302 clinical medicineotorhinolaryngologic diseasesmedicineEvoked Potentials Auditory Brain StemHumansGenetic Predisposition to DiseaseChildAllelesmedicine.diagnostic_testbusiness.industryAudiogramSequence Analysis DNAmedicine.diseaseMinor allele frequency030104 developmental biologyOtorhinolaryngologyMutationAudiometry Pure-ToneSensorineural hearing lossFemaleAudiometrymedicine.symptombusinessCarrier Proteins030217 neurology & neurosurgeryEar and hearing
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Association between familial hypobetalipoproteinemia and the risk of diabetes. Is this the other side of the cholesterol-diabetes connection? A syste…

2017

Statin therapy is beneficial in reducing LDL cholesterol (LDL-C) levels and cardiovascular events, but it is associated with the risk of incident diabetes mellitus (DM). Familial hypercholesterolemia (FH) is characterized by genetically determined high levels of plasma LDL-C and a low prevalence of DM. LDL-C levels seem then inversely correlated with prevalence of DM. Familial hypobetalipoproteinemia (FHBL) represents the genetic mirror of FH in terms of LDL-C levels, very low in subjects carrying mutations of APOB, PCSK9 (FHBL1) or ANGPTL3 (FHBL2). This review explores the hypothesis that FHBL might represent also the genetic mirror of FH in terms of prevalence of DM and that it is expecte…

0301 basic medicineProbandMalemedicine.medical_specialtySettore MED/09 - Medicina InternaApolipoprotein BEndocrinology Diabetes and MetabolismPopulationPrevalenceFamilial hypercholesterolemia030204 cardiovascular system & hematologyHypobetalipoproteinemias03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEndocrinologyInternal medicineDiabetes mellitusInternal MedicinemedicineDiabetes MellitusPrevalenceHumansFamilial hypobetalipoproteinemiaDiabetes mellitus riskeducationeducation.field_of_studybiologyCholesterolbusiness.industryPCSK9StatinsStatinGeneral MedicineCholesterol LDLFamilial hypobetalipoproteinemia; Cholesterol; Diabetes mellitus risk ;Statinsmedicine.diseaseFamilial hypobetalipoproteinemia-Cholesterol- Diabetes mellitus risk- Statins030104 developmental biologyEndocrinologyCholesterolchemistrybiology.proteinlipids (amino acids peptides and proteins)Femalebusiness
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Trio Clinical Exome Sequencing in a Patient With Multicentric Carpotarsal Osteolysis Syndrome: First Case Report in the Balkans

2018

Exome sequencing can interrogate thousands of genes simultaneously and it is becoming a first line diagnostic tool in genomic medicine. Herein, we applied trio clinical exome sequencing in a patient presenting with undiagnosed skeletal disorder, minor facial abnormalities, and kidney hypoplasia; her parents were asymptomatic. Testing the proband and her parents led to the identification of a de novo mutation c.188C>T (p.Pro63Leu) in the MAFB gene, which is known to cause multicentric carpotarsal osteolysis syndrome (MCTO). The c.188C>T mutation lies in a hotspot amino acid stretch within the transactivation domain of MAFB, which is a negative regulator of RANKL-induced osteoclastogenesis. M…

0301 basic medicineProbandOsteolysislcsh:QH426-470030105 genetics & heredityBioinformaticsAsymptomaticDNA sequencingNephropathy03 medical and health sciencesSkeletal disorderBalkanmedicineGeneticscase reportGenetics (clinical)Exome sequencingbusiness.industrymulticentric carpotarsal osteolysis syndromemedicine.diseaselcsh:Genetics030104 developmental biologyMAFBMolecular Medicinenext-generation sequencingmedicine.symptombusinessexome sequencingFrontiers in Genetics
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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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Inter-familial and intra-familial phenotypic variability in three Sicilian families with Anderson-Fabry disease.

2017

// Antonino Tuttolomondo 1 , Irene Simonetta 1 , Giovanni Duro 2 , Rosaria Pecoraro 1 , Salvatore Miceli 1 , Paolo Colomba 2 , Carmela Zizzo 2 , Antonia Nucera 3, 4 , Mario Daidone 1 , Tiziana Di Chiara 1 , Rosario Scaglione 1 , Vittoriano Della Corte 1 , Francesca Corpora 1 , Danai Vogiatzis 1 and Antonio Pinto 1 1 U.O.C di Medicina Interna con Stroke Care, Dipartimento Biomedico di Medicina Interna e Specialistica (Di.Bi.M.I.S), University of Palermo, Palermo, Italy 2 CNR-IBIM: Institute of Biomedicine and Molecular Immunology “A. Monroy” Palermo, Palermo, Italy 3 Stroke Unit, Neurology, Saint Andrea Hospital, La Spezia, Italy 4 Department of Clinical Neurological Sciences, Western Univer…

0301 basic medicineProbandmedicine.medical_specialtyPediatricsNeurologyfamilySettore MED/09 - Medicina InternaDiseaseGene mutationAnderson-Fabry disease (AFD)Pathogenesis03 medical and health sciences0302 clinical medicineAnderson-Fabry disease (AFD); family; variabilitymedicineGeneticsbusiness.industryvariabilityOrgan dysfunctionmedicine.diseaseFabry diseaselanguage.human_language030104 developmental biologyOncologylanguagemedicine.symptombusinessSicilian030217 neurology & neurosurgeryResearch Paper
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