Search results for "polymorph"

showing 10 items of 2115 documents

Mean Platelet Volume and Arterial Stiffness - Clinical Relationship and Common Genetic Variability

2017

AbstractVessel wall stiffening is an important clinical parameter, but it is unknown whether platelets, key elements in the pathogenesis of arterial thrombosis, are associated with arterial stiffness. The present studies sought to determine whether mean platelet volume (MPV), a potential marker of platelet activation, is linked to vascular elasticity as assessed by the augmentation index (AIx), in 15,010 individuals from the population-based Gutenberg Health Study. Multivariable analysis showed that MPV in both males (β 0.776; 95thCI [0.250;1.16]; p = 0.0024) and females (β 0.881[0.328;1.43]; p = 0.0018) is strongly associated with AIx. Individuals with MPV and AIx above the sex-specific me…

Male0301 basic medicinemedicine.medical_specialtyPopulationKaplan-Meier Estimate030204 cardiovascular system & hematologyPolymorphism Single NucleotideArticle03 medical and health sciencesSex FactorsVascular Stiffness0302 clinical medicineGUTENBERG HEALTHDEFICIENTINFLAMMATIONRisk FactorsInternal medicinemedicineHumansPlateletPlatelet activationMean platelet volumeeducationMETAANALYSISeducation.field_of_studyMultidisciplinaryHYPERTENSIONbusiness.industryProportional hazards modelHazard ratioGenetic VariationCROSS-SECTIONAL RELATIONSmedicine.diseaseThrombosisElasticityREACTIVITY030104 developmental biologyISCHEMIC-STROKEATHEROSCLEROSISCardiovascular DiseasesArterial stiffnessCardiologyFemalebusinessMean Platelet VolumeVASCULAR FUNCTIONBiomarkers
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Intragenic FMR1 disease-causing variants: a significant mutational mechanism leading to Fragile-X syndrome

2017

International audience; Fragile-X syndrome (FXS) is a frequent genetic form of intellectual disability (ID). The main recurrent mutagenic mechanism causing FXS is the expansion of a CGG repeat sequence in the 5'-UTR of the FMR1 gene, therefore, routinely tested in ID patients. We report here three FMR1 intragenic pathogenic variants not affecting this sequence, identified using high-throughput sequencing (HTS): a previously reported hemizygous deletion encompassing the last exon of FMR1, too small to be detected by array-CGH and inducing decreased expression of a truncated form of FMRP protein, in three brothers with ID (family 1) and two splice variants in boys with sporadic ID: a de novo …

Male0301 basic medicinemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesdiagnosisRNA SplicingBiologymedicine.disease_causePolymorphism Single NucleotideArticleFragile X Mental Retardation Protein03 medical and health sciencesExonGenetic linkageplacebo-controlled trial[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyMolecular geneticsGeneticsmedicineHumansgeneGenetics (clinical)GeneticsMutationintron 10SiblingsMiddle Agedmedicine.diseaseFMR1Human genetics3. Good healthFragile X syndromedevelopmental delayof-the-literature030104 developmental biologyintellectual disabilityFragile X SyndromeMutationmental-retardationMedical geneticsFemalepoint mutationdouble-blind[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Patients experiencing statin-induced myalgia exhibit a unique program of skeletal muscle gene expression following statin re-challenge

2017

Statins, the 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase inhibitors, are widely prescribed for treatment of hypercholesterolemia. Although statins are generally well tolerated, up to ten percent of statin-treated patients experience myalgia symptoms, defined as muscle pain without elevated creatinine phosphokinase (CPK) levels. Myalgia is the most frequent reason for discontinuation of statin therapy. The mechanisms underlying statin myalgia are not clearly understood. To elucidate changes in gene expression associated with statin myalgia, we compared profiles of gene expression in skeletal muscle biopsies from patients with statin myalgia who were undergoing statin re-challenge (cases)…

Male0301 basic medicinemyalgiaGene Expressionlcsh:MedicineApoptosis030204 cardiovascular system & hematologyPathology and Laboratory MedicineBioinformaticsBiochemistry0302 clinical medicineMedicine and Health SciencesGene Regulatory Networkslcsh:ScienceMusculoskeletal SystemEnergy-Producing OrganellesMyositisRegulation of gene expressionMultidisciplinaryCell DeathbiologyMusclesDrugsMiddle AgedMitochondriaCell ProcessesHMG-CoA reductaseFemalelipids (amino acids peptides and proteins)AnatomyCellular Structures and Organellesmedicine.symptomResearch ArticleSenescencemedicine.medical_specialtyStatinmedicine.drug_classPainBioenergeticsPolymorphism Single Nucleotide03 medical and health sciencesSigns and SymptomsDiagnostic MedicineInternal medicineGeneticsmedicineHumansGene Regulationcardiovascular diseasesMuscle SkeletalAgedPharmacologybusiness.industrylcsh:RStatinsBiology and Life SciencesComputational Biologynutritional and metabolic diseasesMyalgiaCell Biologymedicine.disease030104 developmental biologyEndocrinologyGene Expression RegulationSkeletal MusclesLeukocytes Mononuclearbiology.proteinProtein prenylationlcsh:QHydroxymethylglutaryl-CoA Reductase InhibitorsSLCO1B1businessPLOS ONE
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NS5A gene analysis by next generation sequencing in HCV nosocomial transmission clusters of HCV genotype 1b infected patients

2019

Background: The aim of the study was to investigate the intra-host variability through next-generation-sequencing (NGS) of the NS5A-gene in nosocomial transmission-clusters observed in two Italian hospitals among hepatitis C virus (HCV)-genotype-1b infected patients. Methods: HCV-sequencing was performed by Sanger-sequencing (NS3 + NS5A + NS5B) and by NGS (NS5A, MiSeq-Illumina) in 15 HCV-1b infected patients [five acute with onco-hematologic-disease and 10 (4/6 acute/chronic) with &beta

Male0301 basic medicinevirusesDrug ResistanceHepacivirusViral Nonstructural Proteinsmedicine.disease_causeSettore MED/42 - Igiene Generale E ApplicataGastroenterologySettore MED/07chemistry.chemical_compound0302 clinical medicineGenotype 1bMedicineVirallcsh:QH301-705.5PhylogenyCross Infectionnosocomial transmissionGastroenterologyHigh-Throughput Nucleotide Sequencingvirus diseasesHCV; NGS; acute infection; chronic infection; nosocomial transmission; sequencing; Acute Disease; Adult; Amino Acid Substitution; Antiviral Agents; Blood Transfusion; Chronic Disease; Cross Infection; Drug Resistance Viral; Female; Genotype; Hepacivirus; Hepatitis C; High-Throughput Nucleotide Sequencing; Host-Pathogen Interactions; Humans; Interferons; Male; Middle Aged; Phylogeny; Polymorphism Single Nucleotide; Viral Nonstructural Proteins; beta-ThalassemiaSingle NucleotideGeneral MedicinesequencingMiddle AgedHepatitis CNGSAcute DiseaseHost-Pathogen InteractionsHCVFemale030211 gastroenterology & hepatologyAdultmedicine.medical_specialtyGenotypeHepatitis C virusViral quasispeciesPolymorphism Single NucleotideAntiviral AgentsArticleDNA sequencing03 medical and health sciencesInternal medicineDrug Resistance ViralHumansBlood TransfusionPolymorphismNS5ANS5BGeneHepatologybusiness.industryNosocomial transmissionbeta-Thalassemiabiochemical phenomena metabolism and nutritionchronic infectionVirologydigestive system diseasesChronic infection030104 developmental biologyAmino Acid Substitutionchemistrylcsh:Biology (General)Chronic DiseaseHCV; NGS; acute infection; chronic infection; nosocomial transmission; sequencingInterferonsbusinessacute infectionDigestive and Liver Disease
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Genetic prediction of ICU hospitalization and mortality in COVID‐19 patients using artificial neural networks

2021

There is an unmet need of models for early prediction of morbidity and mortality of Coronavirus disease-19 (COVID-19). We aimed to a) identify complement-related genetic variants associated with the clinical outcomes of ICU hospitalization and death, b) develop an artificial neural network (ANN) predicting these outcomes and c) validate whether complement-related variants are associated with an impaired complement phenotype. We prospectively recruited consecutive adult patients of Caucasian origin, hospitalized due to COVID-19. Through targeted next-generation sequencing, we identified variants in complement factor H/CFH, CFB, CFH-related, CFD, CD55, C3, C5, CFI, CD46, thrombomodulin/THBD, …

Male0304 Medicinal and Biomolecular Chemistry 0601 Biochemistry and Cell Biology 1103 Clinical SciencesBiochemistry & Molecular BiologyGreeceModels GeneticThrombomodulinCOVID-19Complement System ProteinsCell BiologyMiddle AgedPolymorphism Single NucleotideHospitalizationSettore ICAR/09 - Tecnica Delle CostruzioniIntensive Care UnitsComplement Factor HHumansMolecular MedicineFemaleNeural Networks ComputerMorbidityartificial intelligence complement complement inhibition COVID-19 genetic susceptibility SARS-CoV2Complement ActivationJournal of Cellular and Molecular Medicine
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Association between the polymorphisms of TLR4 and CD14 genes and Alzheimer's disease.

2008

Alzheimer's disease (AD) is a heterogeneous and progressive neurodegenerative disease which in Western society mainly accounts for clinical dementia. Inflammation plays a key role in AD and dissecting the genetics of inflammation may provide an answer to the possible treatment. Hence, the better understanding of different molecular and cellular inflammatory mechanisms is crucial for complete knowledge of AD pathophysiology, and for its prevention and drug therapy. Accordingly, in the present study we evaluated whether the pro-inflammatory polymorphisms of lipopolysaccaride-receptors, +896A/G Toll-Like Receptor (TLR4) and -260C/T CD14, are risk factors for AD. The study included both 626 AD …

MaleALZHEIMER'S DISEASEINFLAMMATIONINNATE IMMUNITYTLR4CD14Lipopolysaccharide ReceptorsInflammationSingle-nucleotide polymorphismDiseaseSystemic inflammationPolymorphism Single NucleotideSeverity of Illness IndexDegenerative diseaseINFLAMMATIONAlzheimer DiseaseRisk FactorsDrug DiscoverymedicineDementiaSNPHumansTLR4AgedPharmacologyAged 80 and overbusiness.industryMiddle Agedmedicine.diseaseToll-Like Receptor 4ItalyALZHEIMER'S DISEASEImmunologyINNATE IMMUNITYFemalemedicine.symptomAlzheimer's diseasebusinessCD14
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Exome sequencing of a family with lone, autosomal dominant atrial flutter identifies a rare variation in ABCB4 significantly enriched in cases

2015

Background Lone atrial flutter (AFL) and atrial fibrillation (AF) are common and sometimes consequential cardiac conduction disorders with a strong heritability, as underlined by recent genome-wide association studies that identified genetic modifiers. Follow-up family-based genetic analysis also identified Mendelian transmission of disease alleles. Three affected members were exome-sequenced for the identification of potential causative mutations, which were subsequently validated by direct sequencing in the other 3 affected members. Taqman assay was then used to confirm the role of any mutation in an independent population of sporadic lone AFL/AF cases. Results The family cluster analysis…

MaleATP Binding Cassette Transporter Subfamily BDNA Mutational AnalysisPopulationMutation MissenseSNPGenome-wide association studySingle-nucleotide polymorphismAtrial flutterBiologyBioinformaticsPolymorphism Single NucleotideDNA Mutational AnalysiExome-sequencingGeneticCardiac conductionGeneticsHumansGenetics(clinical)ExomeAlleleeducationExomeATP-binding cassette B4 (ABCB4)Genetics (clinical)Exome sequencingAgedGenetic associationAged 80 and overGeneticseducation.field_of_studyP-GlycoproteinAtrial fibrillationPedigreeFemaleHumanGenome-Wide Association StudyResearch ArticleSNPs
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Linkage to chromosome 1p36 for attention-deficit/hyperactivity disorder traits in school and home settings.

2008

Contains fulltext : 69485.pdf (Publisher’s version ) (Closed access) BACKGROUND: Limited success has been achieved through previous attention-deficit/hyperactivity disorder (ADHD) linkage scans, which were all designed to map genes underlying the dichotomous phenotype. The International Multi-centre ADHD Genetics (IMAGE) project performed a whole genome linkage scan specifically designed to map ADHD quantitative trait loci (QTL). METHODS: A set of 1094 single selected Caucasian ADHD nuclear families was genotyped on a highly accurate and informative single nucleotide polymorphism (SNP) panel. Two quantitative traits measuring the children's symptoms in home and school settings were collecte…

MaleAdolescentGenetics and epigenetic pathways of disease [NCMLS 6]Genetic LinkageMedizin610 Medicine & healthSingle-nucleotide polymorphismLocus (genetics)Quantitative trait locusNeuroinformatics [DCN 3]Social EnvironmentMental health [NCEBP 9]ArticleWhite PeopleDyslexiaGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciences0302 clinical medicineCognitive neurosciences [UMCN 3.2]Genetic linkagemental disordersmedicinePerception and Action [DCN 1]HumansAttention deficit hyperactivity disorderddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersChildBiological PsychiatryGenetics0303 health sciencesSchools030305 genetics & heredityDyslexia10058 Department of Child and Adolescent PsychiatryHeritabilitymedicine.disease030227 psychiatryPhenotypeGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with HyperactivityChromosomes Human Pair 1Child PreschoolTraitFemalePsychology2803 Biological PsychiatryFunctional Neurogenomics [DCN 2]
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Identification of Novel pro-α2(IX) Collagen Gene Mutations in Two Families with Distinctive Oligo-Epiphyseal Forms of Multiple Epiphyseal Dysplasia

1999

Multiple epiphyseal dysplasia (MED) is a genetically heterogeneous disorder with marked clinical and radiographic variability. Traditionally, the mild "Ribbing" and severe "Fairbank" types have been used to define a broad phenotypic spectrum. Mutations in the gene encoding cartilage oligomeric-matrix protein have been shown to result in several types of MED, whereas mutations in the gene encoding the alpha2 chain of type IX collagen (COL9A2) have so far been found only in two families with the Fairbank type of MED. Type IX collagen is a heterotrimer of pro-alpha chains derived from three distinct genes-COL9A1, COL9A2, and COL9A3. In this article, we describe two families with distinctive ol…

MaleAdolescentRNA SplicingMutantGene mutationBiologyOsteochondrodysplasiasmedicine.disease_causeMultiple epiphyseal dysplasia03 medical and health sciencesExon0302 clinical medicineOsteoarthritismedicineGeneticsHumansGenetics(clinical)Genetic TestingOsteochondrodysplasiaMultiple epiphyseal dysplasiaGene mutationAlleleChildPolymorphism Single-Stranded ConformationalGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesMutationType IX collagenGenetic heterogeneitymedicine.diseaseOsteochondrodysplasiaPedigreeRadiographyCartilageChild PreschoolMutationFemaleEpiphysesProcollagen030217 neurology & neurosurgeryResearch ArticleThe American Journal of Human Genetics
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Childhood gene-environment interactions and age-dependent effects of genetic variants associated with refractive error and myopia: The CREAM Consorti…

2018

Myopia, currently at epidemic levels in East Asia, is a leading cause of untreatable visual impairment. Genome-wide association studies (GWAS) in adults have identified 39 loci associated with refractive error and myopia. Here, the age-of-onset of association between genetic variants at these 39 loci and refractive error was investigated in 5200 children assessed longitudinally across ages 7-15 years, along with gene-environment interactions involving the major environmental risk-factors, nearwork and time outdoors. Specific variants could be categorized as showing evidence of: (a) early-onset effects remaining stable through childhood, (b) early-onset effects that progressed further with i…

MaleAdolescentRefractive ErrorsPolymorphism Single NucleotideArticleWhite PeopleAsian PeopleMyopiaHumansFemaleGene-Environment InteractionGenetic Predisposition to DiseaseLongitudinal StudiesAge of OnsetChildGenome-Wide Association Study
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