Search results for "Phenotype"

showing 10 items of 1875 documents

Kosaki overgrowth syndrome: A novel pathogenic variant in PDGFRB and expansion of the phenotype including cerebrovascular complications

2020

Heterozygous activating variants in platelet-derived growth factor, beta (PDGFRB) are associated with phenotypes including Kosaki overgrowth syndrome (KOGS), Penttinen syndrome and infantile myofibromatosis (IM). Here, we present three new cases of KOGS, including a patient with a novel de novo variant c.1477A > T p.(Ser493Cys), and the oldest known individual age 53 years. The KOGS phenotype includes characteristic facial features, tall stature, scoliosis, hyperelastic thin skin, lipodystrophy, variable intellectual and neurological deterioration, and abnormalities on brain imaging. Long-term outcome is unknown. Our cases confirm the phenotypic spectrum includes progressive flexion contrac…

AdultMale0301 basic medicinePathologymedicine.medical_specialtyInfantile myofibromatosisPDGFRBScoliosis030105 genetics & heredityCraniosynostosisReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesCamptodactylyGeneticsmedicineHumansJoint dislocationStrokeGrowth DisordersGenetics (clinical)business.industryGenetic VariationMiddle Agedmedicine.diseaseCerebrovascular DisordersPhenotype030104 developmental biologymedicine.symptomLipodystrophybusinessClinical Genetics
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Molecular characterization of congenital myasthenic syndromes in Spain.

2017

Congenital myasthenic syndromes (CMS) are a heterogeneous group of genetic disorders, all of which impair neuromuscular transmission. Epidemiological data and frequencies of gene mutations are scarce in the literature. Here we describe the molecular genetic and clinical findings of sixty-four genetically confirmed CMS patients from Spain. Thirty-six mutations in the CHRNE, RAPSN, COLQ, GFPT1, DOK7, CHRNG, GMPPB, CHAT, CHRNA1, and CHRNB1 genes were identified in our patients, with five of them not reported so far.. These data provide an overview on the relative frequencies of the different CMS subtypes in a large Spanish population. CHRNE mutations are the most common cause of CMS in Spain, …

AdultMale0301 basic medicineSlow-channel syndromeAdolescentNeuromuscular transmissionGMPPBGene mutationCOLQCongenital myasthenic syndromeYoung Adult03 medical and health sciences0302 clinical medicineDOK7COLQmedicineHumansCHRNECHRNEGeneGenetics (clinical)health care economics and organizationsMyasthenic Syndromes CongenitalGeneticsbiologyRAPSNMiddle AgedCongenital myasthenic syndromemedicine.diseasePhenotype3. Good healthGenetic mutationsRAPSN030104 developmental biologyGFPT1NeurologySpainPediatrics Perinatology and Child Healthbiology.proteinFemaleNeurology (clinical)030217 neurology & neurosurgery
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Circulating miR-323-3p is a biomarker for cardiomyopathy and an indicator of phenotypic variability in Friedreich’s ataxia patients

2017

AbstractMicroRNAs (miRNAs) are noncoding RNAs that contribute to gene expression modulation by regulating important cellular pathways. In this study, we used small RNA sequencing to identify a series of circulating miRNAs in blood samples taken from Friedreich’s ataxia patients. We were thus able to develop a miRNA biomarker signature to differentiate Friedreich’s ataxia (FRDA) patients from healthy people. Most research on FDRA has focused on understanding the role of frataxin in the mitochondria, and a whole molecular view of pathological pathways underlying FRDA therefore remains to be elucidated. We found seven differentially expressed miRNAs, and we propose that these miRNAs represent …

AdultMale0301 basic medicineSmall RNAAtaxiaSciencePopulationCardiomyopathyBioinformaticsArticleYoung Adult03 medical and health sciencesmicroRNAmedicineHumanseducationCells CulturedAgedCell ProliferationGeneticseducation.field_of_studyMultidisciplinarybiologyQRHigh-Throughput Nucleotide SequencingMiddle AgedPrognosismedicine.diseasePhenotypeMicroRNAs030104 developmental biologyBiological Variation PopulationFriedreich AtaxiaCase-Control StudiesFrataxinbiology.proteinBiomarker (medicine)MedicineFemalemedicine.symptomCardiomyopathiesBiomarkersFollow-Up StudiesScientific Reports
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A constitutive BCL2 down-regulation aggravates the phenotype of PKD1-mutant-induced polycystic kidney disease

2017

IF 5.340; International audience; The main identified function of BCL2 protein is to prevent cell death by apoptosis. Mice knock-out for Bcl2 demonstrate growth retardation, severe polycystic kidney disease (PKD), gray hair and lymphopenia, and die prematurely after birth. Here, we report a 40-year-old male referred to for abdominal and thoracic aortic dissection with associated aortic root aneurysm, PKD, lymphocytopenia with a history of T cell lymphoblastic lymphoma, white hair since the age of 20, and learning difficulties. PKD, which was also detected in the father and sister, was related to an inherited PKD1 mutation. The combination of PKD with gray hair and lymphocytopenia was also r…

AdultMale0301 basic medicineTRPP Cation Channelsphenotypebcl2 geneBiologymicro rnaMice03 medical and health sciencesdown-regulationsymptom aggravating factorshemic and lymphatic diseasest-lymphocyteGene expressionGeneticsmedicinePolycystic kidney diseaseAnimalsHumansGenetic Predisposition to Disease[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsgenesMolecular BiologyGeneGenetics (clinical)Exome sequencingMice KnockoutPKD1apoptosisExonsGeneral MedicinePolycystic Kidney Autosomal Dominantmedicine.diseasePhenotypePedigreeUp-Regulation3. Good healthMicroRNAs030104 developmental biologyMRNA SequencingProto-Oncogene Proteins c-bcl-2[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsImmunologyCancer researchLymphocytopeniapolycystic kidney diseasesbcl-2 proteinHuman Molecular Genetics
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Metabolic disorders and inflammation are associated with familial combined hyperlipemia

2019

Background: Familial Combined Hyperlipidemia (FCH) is related to different metabolic disorders. The objective of this study was to evaluate the presence of alterations of hydrocarbonated metabolism and lipid profile together with inflammatory and adhesion molecules in subjects with FCH compared to controls. Methods: 75 HFC patients and 75 healthy individuals were studied. Glucose, insulin, HOMA-IR index and lipid parameters, in addition to anti-oxidized LDL antibodies (Anti ox-LDL), small and dense LDL (sdLDL) and HDL subfractions, proinflammatory cytokines and adhesion molecules were measured. Results: FCH patients showed higher levels of hydrocarbonated metabolism parameters, total choles…

AdultMale0301 basic medicinemedicine.medical_specialtyApolipoprotein Bmedicine.medical_treatmentPhenotype B of LDL HDL subclassesClinical BiochemistryHyperlipidemia Familial CombinedInflammationBiochemistryProinflammatory cytokine03 medical and health sciences0302 clinical medicineInsulin resistanceInternal medicinemedicineHumansInflammationmedicine.diagnostic_testbiologybusiness.industryCell adhesion moleculeInsulinCholesterol HDLFCHBiochemistry (medical)Insulin resistanceGeneral MedicineMetabolismmedicine.diseasePhenotype030104 developmental biologyEndocrinology030220 oncology & carcinogenesisbiology.proteinCytokinesFemalelipids (amino acids peptides and proteins)medicine.symptombusinessLipid profileAdhesion moleculesClinica Chimica Acta
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Lomitapide affects HDL composition and function

2016

Abstract Background Lomitapide reduces low-density lipoprotein-cholesterol (LDL-C) but also high-density lipoprotein-cholesterol (HDL-C) levels. The latter may reduce the clinical efficacy of lomitapide. We investigated the effect of lomitapide on HDL-C levels and on cholesterol efflux capacity (CEC) of HDL in patients with homozygous familial hypercholesterolemia (HoFH). Methods and results Four HoFH patients were treated with increasing dosages of lomitapide. Lomitapide decreased LDL-C (range −34 to −89%). Total HDL-C levels decreased (range −16 to −34%) with a shift to buoyant HDL. ABCA1-mediated CEC decreased in all patients (range −39 to −99%). The changes of total, ABCG1- and SR-BI-me…

AdultMale0301 basic medicinemedicine.medical_specialtySettore MED/09 - Medicina InternaHDLHomozygous familial hypercholesterolemiaFamilial hypercholesterolemia030204 cardiovascular system & hematologyHyperlipoproteinemia Type IIYoung Adult03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineHumansMedicineIn patientClinical efficacyHyperlipoproteinemia Type IICholesterolbusiness.industryCholesterol HDLHomozygotenutritional and metabolic diseasesCholesterol LDLCholesterol efflux capacityAtherosclerosismedicine.diseaseCholesterol lowering drugsLomitapideLomitapideCholesterolPhenotypeTreatment Outcome030104 developmental biologyEndocrinologychemistryBenzimidazolesFemalelipids (amino acids peptides and proteins)Composition (visual arts)Cholesterol lowering drugHydroxymethylglutaryl-CoA Reductase InhibitorsLipoproteins HDLCardiology and Cardiovascular MedicinebusinessATP Binding Cassette Transporter 1Atherosclerosis
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Downregulation of miRNA17-92 cluster marks Vγ9Vδ2 T cells from patients with rheumatoid arthritis

2018

Abstract Background We aimed to evaluate the phenotype, function, and microRNA (miRNA)17–92 cluster expression in Vγ9Vδ2 T-cell subsets and the correlation with immune response in rheumatoid arthritis (RA) patients. Methods Peripheral blood from 10 early RA untreated patients and 10 healthy donors (HD) was obtained. Polyclonal Vγ9Vδ2 T-cell lines were generated and analysed by flow cytometry. Analysis of miRNA17–92 cluster expression was performed by real-time polymerase chain reaction (RT-PCR), and expression of mRNA target genes was also studied. Results A remarkable change in the distribution of Vγ9Vδ2 T-cell functional subsets was observed in the peripheral blood of RA patients compared…

AdultMale0301 basic medicinemiRNA17–92lcsh:Diseases of the musculoskeletal systemInflammatory cytokineImmunologyDown-RegulationBiologyγδ T cellsProinflammatory cytokineFlow cytometryArthritis RheumatoidPathogenesis03 medical and health sciences0302 clinical medicineImmune systemRheumatologyT-Lymphocyte SubsetsInflammatory cytokines; miRNA17-92; Rheumatoid arthritis; γδ T cells; Rheumatology; Immunology and Allergy; ImmunologymicroRNAmedicineHumansImmunology and AllergyRheumatoid arthritisRheumatoid arthritiγδ T cellmedicine.diagnostic_testEffectorInterleukinMiddle AgedInflammatory cytokinesPhenotypemiRNA17-92MicroRNAsSettore MED/16 - Reumatologia030104 developmental biology030220 oncology & carcinogenesisImmunologyFemalelcsh:RC925-935Research Article
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Interleukin (IL)-9/IL-9R axis drives γδ T cells activation in psoriatic arthritis patients

2016

Summary Cytokines such as tumour necrosis factor (TNF)-α, interleukin (IL)-12, interferon (IFN)-γ, IL-23 and, more recently, IL-9, have been implicated in the initiation/maintenance of inflammation in psoriasis and psoriatic arthritis (PsA). In the present study we aimed to characterize the role of γδ T cells in peripheral blood and synovial fluid of PsA patients and to investigate their response to in-vitro stimulation with antigen or cytokines (IL-9 and IL-23). γδ T cells isolated from peripheral blood mononuclear cells and synovial fluid were analysed by flow cytometry to evaluate the phenotype and cytokine production. IL-23R and IL-9R gene expression were also evaluated by reverse trans…

AdultMale0301 basic medicinepsoriatic arthritimedicine.medical_treatmentImmunologyInflammationLymphocyte ActivationSeverity of Illness IndexPeripheral blood mononuclear cellImmunophenotypingγδ-T cellsYoung Adult03 medical and health sciences0302 clinical medicineAntigenT-Lymphocyte SubsetsInterferonSynovial FluidmedicineHumansImmunology and AllergySynovial fluidAgedReceptors Interleukin-9psoriatic arthritis030203 arthritis & rheumatologybusiness.industryArthritis PsoriaticInterleukin-9InterleukinReceptors Antigen T-Cell gamma-deltaOriginal ArticlesIL-9; IL-9R; psoriatic arthritis; γδ-T cells; Immunology and Allergy; ImmunologyMiddle AgedIL-9IL-9RSettore MED/16 - ReumatologiaPhenotype030104 developmental biologyCytokineImmunologyFemaleTumor necrosis factor alphamedicine.symptombusinessBiomarkersmedicine.drugClinical and Experimental Immunology
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Chromosome 15q BP3 to BP5 deletion is a likely locus for speech delay and language impairment: Report on a four‐member family and an unrelated boy

2020

Abstract Background Deletions in chromosome 15q13 have been reported both in healthy people and individuals with a wide range of behavioral and neuropsychiatric disturbances. Six main breakpoint (BP) subregions (BP1‐BP6) are mapped to the 15q13 region and three further embedded BP regions (BP3‐BP5). The deletion at BP4‐BP5 is the rearrangement most frequently observed compared to other known deletions in BP3‐BP5 and BP3‐BP4 regions. Deletions of each of these three regions have previously been implicated in a variable range of clinical phenotypes, including minor dysmorphism, developmental delay/intellectual disability, epilepsy, autism spectrum disorders, behavioral disturbances, and speec…

AdultMale0301 basic medicinespeech delayAdolescentlcsh:QH426-470BP3-BP5 deletionspeech delay.Chromosome DisordersLocus (genetics)030105 genetics & heredity03 medical and health sciencesEpilepsySettore MED/38 - Pediatria Generale E SpecialisticaSeizuresIntellectual DisabilityIntellectual disabilitychromosome 15 q13GeneticsmedicineHumansLanguage Development DisordersChildMolecular BiologyGenetics (clinical)GeneticsChromosomes Human Pair 15business.industryBreakpointlanguage impairmentOriginal Articlesmedicine.diseasePhenotypePedigreeBP3‐BP5 deletiondevelopmental delayLanguage developmentlcsh:GeneticsPhenotype030104 developmental biologyBP3-BP5 deletion; chromosome 15 q13; developmental delay; language impairment; speech delaySpeech delayAutismFemaleOriginal ArticleChromosome Deletionmedicine.symptombusinessMolecular Genetics & Genomic Medicine
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Phenotypical features of two patients diagnosed with PHARC syndrome and carriers of a new homozygous mutation in the ABHD12 gene.

2018

Abstract PHARC (Polyneuropathy, Hearing loss, Ataxia, Retinitis pigmentosa and Cataracts) (MIM# 612674 ) is an autosomal recessive neurodegenerative disease caused by mutations in the ABHD12 gene. We evaluated two Spanish siblings affected with pes cavus, sensorimotor neuropathy, hearing loss, retinitis pigmentosa and juvenile cataracts in whom the genetic test of ABHD12 revealed a novel homozygous frameshift mutation, c.211_223del (p.Arg71Tyrfs*26). The earliest clinical manifestation in these patients was a demyelinating neuropathy manifested with a Charcot-Marie-Tooth phenotype over three decades. Progressive hearing loss, cataracts and retinitis pigmentosa appeared after the age of 30. …

AdultMaleARLID12 genecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyAtaxiagenetic structuresHearing lossUsher syndromeCharcot-Marie-Tooth diseaseCataractFrameshift mutation03 medical and health sciencesPolyneuropathies0302 clinical medicineCataractsRetinitis pigmentosaotorhinolaryngologic diseasesmedicineHumansMuscle SkeletalDeaf-blindnessbusiness.industryPHARCBrainmedicine.diseaseDermatologyMagnetic Resonance Imagingeye diseasesMonoacylglycerol LipasesPedigreePhenotypeNeurologySpainMutation030221 ophthalmology & optometryAtaxiasense organsNeurology (clinical)medicine.symptombusinessUsher syndromePolyneuropathy030217 neurology & neurosurgeryRetinitis PigmentosaRetinopathyJournal of the neurological sciences
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