Search results for "Syndrome"

showing 10 items of 4503 documents

Clinical and biochemical characteristics of individuals with low cholesterol syndromes: A comparison between familial hypobetalipoproteinemia and fam…

2017

Background The most frequent monogenic causes of low plasma cholesterol are familial hypobetalipoproteinemia (FHBL1) because of truncating mutations in apolipoprotein B coding gene (APOB) and familial combined hypolipidemia (FHBL2) due to loss-of-function mutations in ANGPTL3 gene. Objective A direct comparison of lipid phenotypes of these 2 conditions has never been carried out. In addition, although an increased prevalence of liver steatosis in FHBL1 has been consistently reported, the hepatic consequences of FHBL2 are not well established. Methods We investigated 350 subjects, 67 heterozygous carriers of APOB mutations, 63 carriers of the p.S17* mutation in ANGPTL3 (57 heterozygotes and …

0301 basic medicineMaleHepatic steatosisSettore MED/09 - Medicina InternaApolipoprotein BEndocrinology Diabetes and Metabolism030204 cardiovascular system & hematologymedicine.disease_causeANGPTL3 gene; APOB gene; Familial combined hypolipidemia; Familial hypobetalipoproteinemia; HDL cholesterol; Hepatic steatosis; Low cholesterol syndromesHypobetalipoproteinemiasExon0302 clinical medicineHDL cholesterolANGPTL3Nutrition and DieteticFamilial hypobetalipoproteinemiaGeneticsMutationNutrition and Dieteticsbiologyhepatic steatosisHomozygoteANGPTL3 geneMiddle AgedLow cholesterol syndromesPhenotypePhenotypelipids (amino acids peptides and proteins)FemaleCardiology and Cardiovascular MedicineANGPTL3 gene; APOB gene; familial combined hypolipidemia; familial hypobetalipoproteinemia; HDL cholesterol; hepatic steatosis; low cholesterol syndromesmedicine.medical_specialtyHeterozygoteLow cholesterol syndromeHepatic steatosi03 medical and health sciencesInternal medicineInternal MedicinemedicineHumansAPOB geneFamilial combined hypolipidemiaGeneAgedAngiopoietin-Like Protein 3Apolipoproteins Bbusiness.industryHeterozygote advantagemedicine.disease030104 developmental biologyEndocrinologyAngiopoietin-like ProteinsMutationbiology.proteinlow cholesterol syndromesSteatosisbusiness
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Multicomponent Training Prevents Memory Deficit Related to Amyloid-β Protein-Induced Neurotoxicity.

2021

Background: Alzheimer’s disease (AD) is characterized by the accumulation of the amyloid-β peptide in the brain, leading to early oxidative stress and neurotoxicity. It has been suggested that physical exercise could be beneficial in preventing AD, but studies with multicomponent training are scanty. Objective: Verify the effects of multicomponent exercise training to prevent deficits in recognition memory related to Aβ neurotoxicity. Methods: We subjected Wistar rats to multicomponent training (including aerobic and anaerobic physical exercise and cognitive exercise) and then infused amyloid-β peptide into their hippocampus. Results: We show that long-term multicomponent training prevents …

0301 basic medicineMaleHippocampusPhysical exercisePharmacologyHippocampal formationmedicine.disease_causeHippocampusLipid peroxidationStereotaxic Techniques03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysical Conditioning AnimalMedicineAnimalsRats WistarRecognition memoryMemory DisordersAmyloid beta-Peptidesbusiness.industryGeneral NeuroscienceNeurotoxicityBrainGeneral Medicinemedicine.diseaseRatsPsychiatry and Mental healthClinical PsychologyDisease Models AnimalOxidative Stress030104 developmental biologychemistryNeurotoxicity SyndromesLipid PeroxidationGeriatrics and GerontologybusinessAnaerobic exercise030217 neurology & neurosurgeryOxidative stressJournal of Alzheimer's disease : JAD
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Cardiac electrical defects in progeroid mice and Hutchinson-Gilford progeria syndrome patients with nuclear lamina alterations

2016

This work was supported by Spanish Ministry of Economy and Competitiveness (MINECO) Grants SAF2010-16044 and SAF2013-46663-R (to V.A.), SAF2011-30312 and SAF2014-58286-C2-1-R (to L.H.-M.), SAF2011-30088 (to E.D.), and SAF2014-52413-R (to C.L.-O.) and Fondo de Investigación Sanitaria del Instituto de Salud Carlos III Grants RD12/0042/0028 (to V.A.), RD12/0042/0011 (to J.T.), and RD12/0042/0002 (to L.H.-M.), with cofunding from the Fondo Europeo de Desarrollo Regional and the Progeria Research Foundation. J.A.G. is the recipient of a U-Mobility Grant from the Marie Curie cofunding of Regional, National and International Programme (Grant 246550). The Instituto Universitario de Oncología is sup…

0301 basic medicineMaleHutchinson–Gilford progeria syndrome calcium handling connexin43 prelamin A progerinElectrònica en cardiologia030204 cardiovascular system & hematologyPathogenesisCiencias Biomedicas0302 clinical medicineProgeriaCardiac Conduction System DiseasefisiologiapatologíaTecnología médicaChildCiencias médicasMice KnockoutProgeriaprelamin AMultidisciplinaryintegumentary systemMetalloendopeptidasesHeartProgerinHutchinson-Gilford progeria syndrome3. Good health:Enginyeria biomèdica::Electrònica biomèdica::Electrònica en cardiologia [Àrees temàtiques de la UPC]Sarcoplasmic Reticulummedicine.anatomical_structurePNAS PlusChild Preschoolcardiovascular systemNuclear laminaFemalemedicine.symptomBradycardiaAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesAdolescentBiology03 medical and health sciencesQRS complexYoung AdultElectrònica mèdicaInternal medicinemedicineAnimalsHumansPR intervalHutchinson–Gilford progeria syndromeNuclear LaminaMyocardiumMembrane Proteinsnutritional and metabolic diseasesArrhythmias Cardiacmedicine.diseaseMedical electronicsconnexin43Mice Inbred C57BL030104 developmental biologyEndocrinologyVentricleprogerinConnexin 43calcium handlingsistema cardiovascularCalcium
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The oculoauriculofrontonasal syndrome: Further clinical characterization and additional evidence suggesting a nontraditional mode of inheritance

2018

IF 2.264; International audience; The oculoauriculofrontonasal syndrome (OAFNS) is a rare disorder characterized by the association of frontonasal dysplasia (widely spaced eyes, facial cleft, and nose abnormalities) and oculo-auriculo-vertebral spectrum (OAVS)-associated features, such as preauricular ear tags, ear dysplasia, mandibular asymmetry, epibulbar dermoids, eyelid coloboma, and costovertebral anomalies. The etiology is unknown so far. This work aimed to identify molecular bases for the OAFNS. Among a cohort of 130 patients with frontonasal dysplasia, accurate phenotyping identified 18 individuals with OAFNS. We describe their clinical spectrum, including the report of new features…

0301 basic medicineMaleInheritance Patterns030105 genetics & heredityfrontonasal dysplasiawhole exome sequencingCraniofacial Abnormalities0302 clinical medicinePolymicrogyriaEye AbnormalitiesEar External10. No inequalityChildGenetics (clinical)Exome sequencingwhole genome sequencingThyroid agenesisHypoplasiaDNA-Binding ProteinsPhenotypeChild PreschoolFemaleRespiratory System Abnormalitiesmedicine.medical_specialtyAdolescentQuantitative Trait LociOculoauriculofrontonasal syndrome03 medical and health sciencesExome SequencingGeneticsmedicineHumansGenetic Predisposition to DiseaseFrontonasal dysplasiaGenetic Association StudiesWhole genome sequencingHomeodomain Proteinsbusiness.industryFacial cleftSkullInfant NewbornFaciesInfant030206 dentistrymedicine.diseaseDermatologySpine[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsDysplasiabusinessTomography Spiral ComputedTranscription Factors
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Pistachio Consumption Alleviates Inflammation and Improves Gut Microbiota Composition in Mice Fed a High-Fat Diet.

2019

High-fat diet (HFD) induces inflammation and microbial dysbiosis, which are components of the metabolic syndrome. Nutritional strategies can be a valid tool to prevent metabolic and inflammatory diseases. The aim of the present study was to evaluate if the chronic intake of pistachio prevents obesity-associated inflammation and dysbiosis in HFD-fed mice. Three groups of male mice (four weeks old

0301 basic medicineMaleInterleukin-1betaAdipose tissueGut floralcsh:ChemistryMice0302 clinical medicineLactobacilluslcsh:QH301-705.5SpectroscopyChemokine CCL2biologydigestive oral and skin physiologyfood and beveragesGeneral Medicinepistachio intakeobesity-related inflammation pistachio intake gut microbiota HFD mice adipose tissueComputer Science Applicationsadipose tissueLiverPistacialipids (amino acids peptides and proteins)medicine.symptomhormones hormone substitutes and hormone antagonistsmedicine.medical_specialty030209 endocrinology & metabolismInflammationDiet High-FatCatalysisArticleInorganic Chemistry03 medical and health sciencesInternal medicineobesity-related inflammationmedicineAnimalsHFD miceObesityPhysical and Theoretical ChemistryMolecular BiologyFecesgut microbiotaTumor Necrosis Factor-alphaOrganic Chemistrynutritional and metabolic diseasesmedicine.diseasebiology.organism_classificationObesityGastrointestinal MicrobiomeMice Inbred C57BL030104 developmental biologyEndocrinologylcsh:Biology (General)lcsh:QD1-999DysbiosisMetabolic syndromeDysbiosisDiet TherapyInternational journal of molecular sciences
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De Novo and Inherited Pathogenic Variants in KDM3B Cause Intellectual Disability, Short Stature, and Facial Dysmorphism

2019

Contains fulltext : 202646.pdf (Publisher’s version ) (Open Access) By using exome sequencing and a gene matching approach, we identified de novo and inherited pathogenic variants in KDM3B in 14 unrelated individuals and three affected parents with varying degrees of intellectual disability (ID) or developmental delay (DD) and short stature. The individuals share additional phenotypic features that include feeding difficulties in infancy, joint hypermobility, and characteristic facial features such as a wide mouth, a pointed chin, long ears, and a low columella. Notably, two individuals developed cancer, acute myeloid leukemia and Hodgkin lymphoma, in childhood. KDM3B encodes for a histone …

0301 basic medicineMaleJumonji Domain-Containing Histone DemethylasesDevelopmental DisabilitiesWEAVER SYNDROMEPROTEINHaploinsufficiencyCraniofacial AbnormalitiesHistones0302 clinical medicineIntellectual disabilityTumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14]Missense mutationDEMETHYLASE KDM3BExomeChildGenetics (clinical)Exome sequencingGeneticsRUBINSTEIN-TAYBI SYNDROMEMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]Phenotype030220 oncology & carcinogenesisFemalemedicine.symptomHaploinsufficiencyRare cancers Radboud Institute for Health Sciences [Radboudumc 9]Joint hypermobilityGENETICSJMJD1CMutation MissenseDwarfismBiologyShort statureKdm3b ; Cancer Predisposition ; Developmental Delay ; Facial Recognition ; Intellectual Disability ; Leukemia ; Lymphoma ; Short Stature03 medical and health sciencesReportIntellectual DisabilitymedicineHumansMYELOID-LEUKEMIAGenetic Association StudiesGerm-Line MutationWeaver syndromeNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Rubinstein–Taybi syndromeMUTATIONSDELETIONGenetic Variationmedicine.diseaseBody HeightMusculoskeletal AbnormalitiesINDIVIDUALS030104 developmental biologyFaceNanomedicine Radboud Institute for Molecular Life Sciences [Radboudumc 19]American Journal of Human Genetics
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Interleukin-25 Axis Is Involved in the Pathogenesis of Human Primary and Experimental Murine Sjögren's Syndrome

2018

Objective To investigate the role of the interleukin-25 (IL-25)/IL-17 receptor B (IL-17RB) axis in experimental Sjogren's syndrome (SS) and in patients with primary SS and primary SS-associated lymphoma. Methods Expression of IL-25, IL-17RB, IL-17B, and tumor necrosis factor receptor-associated factor 6 (TRAF6) was analyzed on minor salivary gland (SG) samples from patients with primary SS and on parotid gland samples from patients with primary SS-associated B cell non-Hodgkin's lymphoma (NHL). IL-17RB expression and the frequencies of natural group 2 innate lymphoid cells (ILC2s), inflammatory ILC2s, and M2-polarized macrophages were assessed by flow cytometry in SG mononuclear cells and p…

0301 basic medicineMaleLymphomaMacrophageImmunologyPeripheral blood mononuclear cellSalivary GlandSalivary GlandsFlow cytometry03 medical and health sciencesMice0302 clinical medicineRheumatologyInterleukin 25AnimalsHumansMedicineImmunology and AllergyLymphocytesB cellAgedReceptors Interleukin-17medicine.diagnostic_testbusiness.industryAnimalMacrophagesInnate lymphoid cellInterleukin-17Middle Agedmedicine.diseaseImmunity InnateLymphomaSettore MED/16 - Reumatologia030104 developmental biologymedicine.anatomical_structureSjogren's SyndromeImmunologyImmunology and Allergy; Rheumatology; ImmunologyLeukocytes MononuclearRituximabTumor necrosis factor alphaFemaleLymphocytebusiness030215 immunologymedicine.drugHuman
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Dominant variants in the splicing factor PUF60 cause a recognizable syndrome with intellectual disability, heart defects and short stature

2016

Item does not contain fulltext Verheij syndrome, also called 8q24.3 microdeletion syndrome, is a rare condition characterized by ante- and postnatal growth retardation, microcephaly, vertebral anomalies, joint laxity/dislocation, developmental delay (DD), cardiac and renal defects and dysmorphic features. Recently, PUF60 (Poly-U Binding Splicing Factor 60 kDa), which encodes a component of the spliceosome, has been discussed as the best candidate gene for the Verheij syndrome phenotype, regarding the cardiac and short stature phenotype. To date, only one patient has been reported with a de novo variant in PUF60 that probably affects function (c.505C>T leading to p.(His169Tyr)) associated wi…

0301 basic medicineMaleMESH: Heart Defects Congenital / physiopathologyMicrocephalyPathologyMESH: Heart Defects Congenital / geneticsMESH: Exome / genetics030105 genetics & heredityMESH: RNA Splicing / geneticsMicrophthalmia[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesMESH: ChildExomeMESH: RNA Splicing Factors / geneticsChildFrameshift MutationMESH: High-Throughput Nucleotide SequencingGenetics (clinical)Exome sequencingColobomaMESH: Frameshift MutationHigh-Throughput Nucleotide SequencingMicrodeletion syndromeMicrocephaly Verheij syndrome PUF60ChemistryPhenotypeChild PreschoolDISEASESMicrocephalyMedical geneticsFemaleRNA Splicing Factorsmedicine.symptomChromosome DeletionChromosomes Human Pair 8MESH: Dwarfism / genetics*Heart Defects Congenitalmedicine.medical_specialtyGENESAdolescentRNA SplicingMESH: Chromosome DeletionDwarfismBiologyMESH: PhenotypeShort statureArticlePUF6003 medical and health sciencesInternal medicineIntellectual Disability[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineHumansCraniofacialBiologyMESH: AdolescentNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]MESH: HumansMESH: Child Preschoolmedicine.diseaseMESH: Repressor Proteins / geneticsMESH: MaleRepressor Proteins030104 developmental biologyEndocrinologyMESH: Chromosomes Human Pair 8 / geneticsMESH: Dwarfism / physiopathologyMESH: Intellectual Disability / physiopathologyHuman medicineMESH: Intellectual Disability / geneticsVerheij syndromeMESH: Female[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Autosomal-Recessive Mutations in AP3B2, Adaptor-Related Protein Complex 3 Beta 2 Subunit, Cause an Early-Onset Epileptic Encephalopathy with Optic At…

2016

International audience; Early-onset epileptic encephalopathy (EOEE) represents a heterogeneous group of severe disorders characterized by seizures, interictal epileptiform activity with a disorganized electroencephalography background, developmental regression or retardation, and onset before 1 year of age. Among a cohort of 57 individuals with epileptic encephalopathy, we ascertained two unrelated affected individuals with EOEE associated with developmental impairment and autosomal-recessive variants in AP3B2 by means of whole-exome sequencing. The targeted sequencing of AP3B2 in 86 unrelated individuals with EOEE led to the identification of an additional family. We gathered five addition…

0301 basic medicineMaleMicrocephalyDevelopmental DisabilitiesPostnatal microcephalycopper-metabolismEpilepsy0302 clinical medicineexpansionhermansky-pudlak-syndromeddc:576.5Age of OnsetChilddisordersGenetics (clinical)seizuresGeneticsMEDNIK syndromeSyndrome3. Good healthPedigreeintellectual disabilityChild Preschoolmednik syndromeMicrocephalyFemaleDevelopmental regressionAdaptor Protein Complex 3Genes RecessiveBiologyAP3B103 medical and health sciencesAtrophyReport[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineHumansAdaptor Protein Complex beta SubunitsmousediseaseEpilepsyap-4 deficiencyInfant NewbornInfantmedicine.diseaseOptic Atrophy030104 developmental biologyMutationHermansky–Pudlak syndrome030217 neurology & neurosurgery[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Am J Hum Genet

2019

ZMIZ1 is a coactivator of several transcription factors, including p53, the androgen receptor, and NOTCH1. Here, we report 19 subjects with intellectual disability and developmental delay carrying variants in ZMIZ1. The associated features include growth failure, feeding difficulties, microcephaly, facial dysmorphism, and various other congenital malformations. Of these 19, 14 unrelated subjects carried de novo heterozygous single-nucleotide variants (SNVs) or single-base insertions/deletions, 3 siblings harbored a heterozygous single-base insertion, and 2 subjects had a balanced translocation disrupting ZMIZ1 or involving a regulatory region of ZMIZ1. In total, we identified 13 point mutat…

0301 basic medicineMaleMicrocephaly[SDV]Life Sciences [q-bio]Developmental DisabilitiesAucunBiology030226 pharmacology & pharmacyTransactivation03 medical and health sciencesMiceNeurodevelopmental disorder0302 clinical medicineReportIntellectual DisabilityCoactivatormedicineGeneticsAnimalsHumansPoint MutationAlleleChildExomeGenetics (clinical)Alleles030304 developmental biologyGenetics0303 health sciencesPoint mutationCorrectionInfantSyndromemedicine.diseaseAndrogen receptor030104 developmental biologyChild PreschoolFemale030217 neurology & neurosurgeryTranscription Factors
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