Search results for "Bioinformatic"

showing 10 items of 1651 documents

Genome-wide analysis reveals DNA methylation markers that vary with both age and obesity

2014

AbstractThe combination of the obesity epidemic and an aging population presents growing challenges for the healthcare system. Obesity and aging are major risk factors for a diverse number of diseases and it is of importance to understand their interaction and the underlying molecular mechanisms. Herein the authors examined the methylation levels of 27578 CpG sites in 46 samples from adult peripheral blood. The effect of obesity and aging was ascertained with general linear models. More than one hundred probes were correlated to aging, nine of which belonged to the KEGG group map04080. Additionally, 10 CpG sites had diverse methylation profiles in obese and lean individuals, one of which wa…

AdultGenetic Markersmedicine.medical_specialtyAgingAlpha-Ketoglutarate-Dependent Dioxygenase FTOGenome-wide association studyBiologyMicroarrayBioinformaticsEpigenesis GeneticGeneticsmedicineHumansEpigeneticsObesityKEGGTelomeraseAgedMedicinsk genetikGeneticsProteinsGeneral MedicineMethylationDNA MethylationMiddle Agedmedicine.diseaseObesityCpG siteDNA methylationMedical geneticsCpG IslandsFemaleEpigeneticsMedical GeneticsGenome-Wide Association Study
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Search for a gene responsible for Floating-Harbor syndrome on chromosome 12q15q21.1.

2012

International audience; Floating-Harbor syndrome (FHS) is characterized by characteristic facial dysmorphism, short stature with delayed bone age, and expressive language delay. To date, the gene(s) responsible for FHS is (are) unknown and the diagnosis is only made on the basis of the clinical phenotype. The majority of cases appeared to be sporadic but rare cases following autosomal dominant inheritance have been reported. We identified a 4.7 Mb de novo 12q15-q21.1 microdeletion in a patient with FHS and intellectual deficiency. Pangenomic 244K array-CGH performed in a series of 12 patients with FHS failed to identify overlapping deletions. We hypothesized that FHS is caused by haploinsuf…

AdultHeart Septal Defects VentricularMaleCandidate geneFloating Harbor syndrome[SDV.GEN] Life Sciences [q-bio]/GeneticsHaploinsufficiencyBiologyBioinformaticsShort statureCraniofacial Abnormalities03 medical and health sciences12q15q21.1 microdeletion[SDV.BDD] Life Sciences [q-bio]/Development BiologyGeneticsmedicineHumansAbnormalities MultipleGenetic Predisposition to Disease[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyChild[SDV.BDD]Life Sciences [q-bio]/Development BiologyGenetics (clinical)Growth Disorders030304 developmental biologySequence DeletionPhenocopyGenetics0303 health sciencesComparative Genomic Hybridization[SDV.GEN]Life Sciences [q-bio]/GeneticsChromosomes Human Pair 12Genetic heterogeneity030305 genetics & heredityChromosomeHigh-Throughput Nucleotide Sequencinghigh-throughput sequencingmedicine.disease3. Good healthPhenotypeFloating–Harbor syndromeChild PreschoolMutation (genetic algorithm)Femalemedicine.symptomHaploinsufficiency[ SDV.GEN ] Life Sciences [q-bio]/Genetics
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AISF update on the diagnosis and management of adult-onset lysosomal storage diseases with hepatic involvement.

2020

Lysosomal storage diseases (LSDs) are a heterogeneous group of inherited disorders caused by loss-of-function mutations in genes encoding for lysosomal enzymes/proteins. The consequence is a progressive accumulation of substrates in these intracellular organelles, resulting in cellular and tissue damage. The overall incidence is about 1/8000 live births, but is likely underestimated. LSDs are chronic progressive multi-systemic disorders, generally presenting with visceromegaly, and involvement of the central nervous system, eyes, the skeleton, and the respiratory and cardiovascular systems. The age at onset and phenotypic expression are highly variable, according to the specific enzymatic d…

AdultHepatosplenomegalyLysosomal acid lipase deficiencyBioinformaticsOrganomegaly03 medical and health sciencesLiver disease0302 clinical medicinemedicineCholesteryl ester storage disease Enzyme replacement therapy Gaucher disease Lysosomal acid lipase Niemann–Pick disease deficiency Substrate reduction therapyHumansSubstrate reduction therapyEnzyme Replacement TherapySocieties MedicalNiemann-Pick DiseasesAcid sphingomyelinase deficiencyGaucher DiseaseHepatologybusiness.industryGastroenterologyWolman DiseaseEnzyme replacement therapymedicine.diseaseLysosomal Storage DiseasesSphingomyelin PhosphodiesteraseItaly030220 oncology & carcinogenesis030211 gastroenterology & hepatologymedicine.symptombusinessNiemann–Pick diseaseLysosomesVisceromegalyDigestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
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Inflammatory markers and cardiovascular risk in the metabolic syndrome

2011

Elevated blood glucose, obesity, high blood pressure, elevated triglycerides and low high density lipoprotein (HDL) cholesterol are well accepted risk factors in the development of coronary artery disease. Clustering of at least three of these factors in an individual is defined as metabolic syndrome (MetS). Obesity is a central pathological mechanism in the disease and it is expected that the incidence of this condition will increase dramatically within the next years. The visceral adipose tissue is not only an energy depot but also an endocrine organ which produces a large number of bioactive molecules, the so called adipokines. In the setting of obesity, the over-production of proinflamm…

AdultLeptinRiskAdolescentAngiotensinogenAdipokineAdipose tissueDiseaseIntra-Abdominal FatBioinformaticsCoronary artery diseasePathogenesisInsulin resistancePlasminogen Activator Inhibitor 1medicineHumansResistinObesityLife StyleChemokine CCL2InflammationMetabolic SyndromeInterleukin-6Tumor Necrosis Factor-alphabusiness.industryAtherosclerosisPrognosismedicine.diseaseObesityPlaque AtheroscleroticCardiovascular DiseasesAdiponectinEndothelium VascularInsulin ResistanceMetabolic syndromebusinessBiomarkersFrontiers in Bioscience
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Further delineation of a rare recessive encephalomyopathy linked to mutations in GFER thanks to data sharing of whole exome sequencing data

2017

Background Alterations in GFER gene have been associated with progressive mitochondrial myopathy, congenital cataracts, hearing loss, developmental delay, lactic acidosis and respiratory chain deficiency in 3 siblings born to consanguineous Moroccan parents by homozygosity mapping and candidate gene approach (OMIM#613076). Next generation sequencing recently confirmed this association by the finding of compound heterozygous variants in 19-year-old girl with a strikingly similar phenotype, but this ultra-rare entity remains however unknown from most of the scientific community. Materials and methods Whole exome sequencing was performed as part of a "diagnostic odyssey" for suspected mitochon…

AdultMale0301 basic medicineHeterozygoteCandidate geneAdolescentdata sharingMitochondrial diseaseCompound heterozygosityBioinformaticsYoung Adult03 medical and health sciencesMitochondrial myopathyMitochondrial EncephalomyopathiesExome SequencingGeneticsHumansMedicineGenetic Predisposition to DiseaseOxidoreductases Acting on Sulfur Group Donorswhole-exome sequencingChildExomeCytochrome ReductasesGenetics (clinical)Exome sequencing[SDV.GEN]Life Sciences [q-bio]/Geneticsbusiness.industryGFERDisease gene identificationmedicine.diseasePedigree3. Good health030104 developmental biologymitochondrial conditionMutationCongenital cataractsFemale[ SDV.GEN ] Life Sciences [q-bio]/GeneticsbusinessClinical Genetics
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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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Corrigendum to “Short-term changes in light distortion in orthokeratology subjects"

2015

Artigo completo publicado na revista "BioMed Research International, (2015), 1-7" e disponível no RepositóriUM em: http://hdl.handle.net/1822/33375

AdultMaleAdolescentLightmedicine.medical_treatmentVisual AcuityLentes de contactolcsh:MedicineBioinformaticsGeneral Biochemistry Genetics and Molecular BiologyContrast SensitivityCorneaYoung AdultDistortionMyopiamedicineHumansÓpticaScience & TechnologyGeneral Immunology and Microbiologybusiness.industrylcsh:ROrthokeratologyCorneal TopographyGeneral MedicineRefractive ErrorsTerm (time)OptometryFemaleCorrigendumbusinessOrthokeratologic Procedures
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The gene expression profile of cumulus cells reveals altered pathways in patients with endometriosis

2014

PURPOSE: The objective of this experimental study was to compare the global gene expression profile of CC of mature oocytes in 18 patients with severe endometriosis and CC in 18 control patients affected by a severe male factor. METHODS: For each group, the CC were pooled, RNA was extracted and a microarray performed. For validating the microarray, a quantitative real-time PCR was performed in the CC of an independent set of patients with endometriosis (n = 5) and controls (n = 7). RESULTS: 595 differentially expressed genes (320 down-regulated, 275 up-regulated, p < 0.05, fold change ≥1.5) were identified. The most significant changes were observed in genes involved in the chemokine signal…

AdultMaleAdolescentMicroarrayEndometriosisEndometriosisDown-Regulationmacromolecular substancesBiologyBioinformaticsTranscriptomeAndrologyYoung AdultDownregulation and upregulationSettore BIO/13 - Biologia ApplicataGene expressionGeneticsmedicineHumansGenetics (clinical)Cumulus CellsMicroarray analysis techniquesGene Expression Profilingmusculoskeletal neural and ocular physiologygene expression profile cumulus cellObstetrics and GynecologyGeneral Medicinegene expression profile cumulus cells; microarray; EndometriosisMicroarray Analysismedicine.diseaseUp-RegulationGene expression profilingReproductive Physiology and Diseasenervous systemReproductive MedicineCase-Control StudiesOocytesFemaleSignal transductionTranscriptomemicroarraySignal TransductionDevelopmental Biology
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Expanding the clinical phenotype of patients with a ZDHHC9 mutation.

2013

In 2007, 250 families with X-linked intellectual disability (XLID) were screened for mutations in genes on the X-chromosome, and in 4 of these families, mutations in the ZDHHC9 gene were identified. The ID was either isolated or associated with a marfanoid habitus. ZDHHC9 encodes a palmitoyl transferase that catalyzes the posttranslational modification of NRAS and HRAS. Since this first description, no additional patient with a ZDHHC9 mutation has been reported in the literature. Here, we describe a large family in which we identified a novel pathogenic ZDHHC9 nonsense mutation (p.Arg298*) by parallel sequencing of all X-chromosome exons. The mutation cosegregated with the clinical phenotyp…

AdultMaleAdolescentX-linked intellectual disabilityGenetic counselingNonsense mutationNeuropsychological TestsBioinformaticsYoung AdultFatal OutcomeGenes X-LinkedIntellectual DisabilityIntellectual disabilityGeneticsmedicineHumansHRASChildGenetics (clinical)GeneticsMassive parallel sequencingAcrocyanosisbusiness.industryBrainFaciesmedicine.diseaseMagnetic Resonance ImagingPedigreePhenotypeMutation (genetic algorithm)MutationbusinessAcyltransferasesAmerican journal of medical genetics. Part A
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Incomplete penetrance and phenotypic variability of 6q16 deletions including SIM1.

2015

International audience; 6q16 deletions have been described in patients with a Prader-Willi-like (PWS-like) phenotype. Recent studies have shown that certain rare single-minded 1 (SIM1) loss-of-function variants were associated with a high intra-familial risk for obesity with or without features of PWS-like syndrome. Although SIM1 seems to have a key role in the phenotype of patients carrying 6q16 deletions, some data support a contribution of other genes, such as GRIK2, to explain associated behavioural problems. We describe 15 new patients in whom de novo 6q16 deletions were characterised by comparative genomic hybridisation or single-nucleotide polymorphism (SNP) array analysis, including…

AdultMaleAdolescent[SDV]Life Sciences [q-bio]PenetranceBioinformaticsPolymorphism Single NucleotideArticlePregnancyGRIK2Basic Helix-Loop-Helix Transcription FactorsGeneticsHumansSNPObesityChildGeneGenetic Association StudiesGenetics (clinical)GeneticsComparative Genomic Hybridizationbiology[ SDV ] Life Sciences [q-bio]InfantPenetrancePhenotypeRepressor ProteinsChild PreschoolAborted FetusSIM1biology.proteinChromosomes Human Pair 6FemaleHaploinsufficiencyPrader-Willi SyndromeComparative genomic hybridization
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