Search results for "metabolism [NF-kappa B]"

showing 10 items of 123 documents

Modulation of the gut microbiota impacts nonalcoholic fatty liver disease: A potential role for bile acids

2017

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide, yet the pathogenesis of NAFLD is only partially understood. Here, we investigated the role of the gut bacteria in NAFLD by stimulating the gut bacteria via feeding mice the fermentable dietary fiber, guar gum (GG), and suppressing the gut bacteria via chronic oral administration of antibiotics. GG feeding profoundly altered the gut microbiota composition, in parallel with reduced diet-induced obesity and improved glucose tolerance. Strikingly, despite reducing adipose tissue mass and inflammation, GG enhanced hepatic inflammation and fibrosis, concurrent with markedly elevated plasma and hepatic bile acid l…

Male0301 basic medicineobesityGut floraGalactansGastroenterologyBiochemistryantibioticsMannansSTEATOHEPATITISVoeding Metabolisme en Genomicachemistry.chemical_compoundLiver diseaseEndocrinologyNon-alcoholic Fatty Liver DiseaseFibrosisAntibioticsPlant GumsNonalcoholic fatty liver diseaseHeptaic inflammationFIBROSIShepatic fibrosisResearch ArticlesHuman Nutrition & HealthbiologyBile acidHumane Voeding & GezondheidMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]Metabolism and GenomicsAnti-Bacterial Agents3. Good healthIntestineL-CARNITINELiverGUAR GUM[ SDV.BBM.GTP ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]Metabolisme en Genomica[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]Nutrition Metabolism and Genomics[ SDV.MHEP.HEG ] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterologymedicine.medical_specialtymedicine.drug_classBiochemieCelbiologie en ImmunologieQD415-436Gut microbiotaMETABOLISMDiet High-Fatdigestive systemDIET03 medical and health sciencesVoedingINFLAMMATIONINTESTINAL MICROBIOTAInternal medicine[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]medicineAnimalsHepatic inflammationObesityintestineVLAGNutritionInflammationBile acids and saltshepatic inflammationBiological Transport[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyCell BiologyGlucose Tolerance Testmedicine.diseaseTaurocholic acidbiology.organism_classification[SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyGastrointestinal MicrobiomeMice Inbred C57BLMICE030104 developmental biologyEndocrinologychemistryCell Biology and ImmunologySteatohepatitisHepatic fibrosisTRIMETHYLAMINE-N-OXIDEHepatic fibrosis
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“Better explanations” in multiple sclerosis diagnostic workup

2019

BackgroundThe exclusion of other diseases that can mimic multiple sclerosis (MS) is the cornerstone of current diagnostic criteria. However, data on the frequency of MS mimics in real life are incomplete.MethodsA total of 695 patients presenting with symptoms suggestive of MS in any of the 22 RIREMS centers underwent a detailed diagnostic workup, including a brain and spinal cord MRI scan, CSF and blood examinations, and a 3-year clinical and radiologic follow-up.FindingsA total of 667 patients completed the study. Alternative diagnoses were formulated in 163 (24.4%) cases, the most frequent being nonspecific neurologic symptoms in association with atypical MRI lesions of suspected vascular…

Male404241Longitudinal StudieDisease0302 clinical medicineMultiple SclerosiDiagnosisMedicine030212 general & internal medicineProspective StudiesLongitudinal StudiesProspective cohort studymedicine.diagnostic_testMagnetic Resonance Imagingclinical practiceatypical MRI lesionsMS mimicsDisease ProgressionFemaleSettore MED/26 - NeurologiaRadiologyHumanAdultmultiple sclerosis; diagnostic criteria; atypical MRI lesions; MS mimics; clinical practicemedicine.medical_specialtyMultiple Sclerosis2omarkers / metabolism Diagnosis Differential Female Follow-Up Studies Humans Longitudinal Studies Magnetic Resonance Imaging Male Multiple Sclerosis / diagnosis* Prospective StudiesArticleFollow-Up StudieDiagnosis Differential03 medical and health sciencesHumansNeuromyelitis opticabusiness.industryMultiple sclerosisAdult; Biomarkers; Diagnosis Differential; Female; Follow-Up Studies; Humans; Longitudinal Studies; Magnetic Resonance Imaging; Male; Multiple Sclerosis; Prospective StudiesMagnetic resonance imagingOdds ratioBiomarkermedicine.disease101MigraineDifferentialdiagnostic criteriaNeurology (clinical)Differential diagnosisbusiness030217 neurology & neurosurgeryBiomarkersFollow-Up StudiesNeurology
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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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Common variants of the liver fatty acid binding protein gene influence the risk of type 2 diabetes and insulin resistance in Spanish population.

2012

Journal Article; Research Support, Non-U.S. Gov't; SUMMARY The main objective was to evaluate the association between SNPs and haplotypes of the FABP1-4 genes and type 2 diabetes, as well as its interaction with fat intake, in one general Spanish population. The association was replicated in a second population in which HOMA index was also evaluated. METHODS 1217 unrelated individuals were selected from a population-based study [Hortega study: 605 women; mean age 54 y; 7.8% with type 2 diabetes]. The replication population included 805 subjects from Segovia, a neighboring region of Spain (446 females; mean age 52 y; 10.3% with type 2 diabetes). DM2 mellitus was defined in a similar way in b…

MaleAnatomy and PhysiologyEspañaDiabetes Mellitus Tipo 2:Named Groups::Persons::Age Groups::Adult::Middle Aged [Medical Subject Headings]Type 2 diabetesResistencia a la InsulinaVariación Genética:Analytical Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Statistics as Topic::Probability::Risk::Risk Factors [Medical Subject Headings]:Phenomena and Processes::Genetic Phenomena::Genotype::Haplotypes [Medical Subject Headings]:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings]EndocrinologyPolymorphism (computer science)Risk FactorsAnálisis de RegresiónFactores de Riesgo:Geographicals::Geographic Locations::Europe::Spain [Medical Subject Headings]Geneticseducation.field_of_studyMultidisciplinaryAdultoQRMiddle AgedCardiovascular Diseases:Diseases::Nutritional and Metabolic Diseases::Metabolic Diseases::Glucose Metabolism Disorders::Diabetes Mellitus::Diabetes Mellitus Type 2 [Medical Subject Headings]Regression AnalysisMedicineFemale:Phenomena and Processes::Genetic Phenomena::Genotype [Medical Subject Headings]:Phenomena and Processes::Genetic Phenomena::Genetic Variation [Medical Subject Headings]Fatty Acid Binding Protein 3Research ArticleAdult:Phenomena and Processes::Genetic Phenomena::Genetic Variation::Mutation [Medical Subject Headings]GenotypeSciencePopulation:Check Tags::Male [Medical Subject Headings]Single-nucleotide polymorphismEndocrine SystemBiologyFatty Acid-Binding ProteinsPolymorphism Single Nucleotide:Diseases::Nutritional and Metabolic Diseases::Metabolic Diseases::Glucose Metabolism Disorders::Hyperinsulinism::Insulin Resistance [Medical Subject Headings]Insulin resistanceGenetic variation:Named Groups::Persons::Age Groups::Adult [Medical Subject Headings]medicineGeneticsHumans:Named Groups::Persons::Age Groups::Adult::Aged [Medical Subject Headings]education:Diseases::Cardiovascular Diseases [Medical Subject Headings]Biology:Phenomena and Processes::Genetic Phenomena::Genetic Structures::Genome::Genome Components::Genes::Alleles [Medical Subject Headings]AllelesAgedDiabetic Endocrinology:Analytical Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Statistics as Topic::Regression Analysis [Medical Subject Headings]:Phenomena and Processes::Genetic Phenomena::Genetic Variation::Polymorphism Genetic::Polymorphism Single Nucleotide [Medical Subject Headings]Polymorphism GeneticEndocrine PhysiologyHaplotypeGenetic Variation:Phenomena and Processes::Genetic Phenomena::Genetic Variation::Polymorphism Genetic [Medical Subject Headings]medicine.diseaseObesity:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Carrier Proteins::Fatty Acid-Binding Proteins [Medical Subject Headings]:Check Tags::Female [Medical Subject Headings]Diabetes Mellitus Type 2HaplotypesSpainMetabolic DisordersMutationInsulin ResistancePopulation GeneticsPloS one
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Altered lipid metabolism in a Drosophila model of Friedreich's ataxia

2010

13 páginas, 5 figuras.-- et al.

MaleAtaxiaCell SurvivalLipid Metabolism Disordersmedicine.disease_causeNervous SystemAnimals Genetically ModifiedLipid peroxidationchemistry.chemical_compoundDownregulation and upregulationIron-Binding ProteinsLipid dropletGeneticsmedicineAnimalsDrosophila ProteinsHumansMolecular BiologyGenetics (clinical)Membrane GlycoproteinsbiologyCélulas glialesFatty AcidsLipid metabolismArticlesGeneral MedicineCell biologyDisease Models AnimalOxidative Stressmedicine.anatomical_structurechemistryBiochemistryFriedreich AtaxiaFrataxinbiology.proteinNeurogliaDrosophilaLipid Peroxidationmedicine.symptomCarrier ProteinsNeurogliaOxidative stress
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Kidney Stones in Primary Hyperoxaluria: New Lessons Learnt

2013

To investigate potential differences in stone composition with regard to the type of Primary Hyperoxaluria (PH), and in relation to the patient’s medical therapy (treatment naïve patients versus those on preventive medication) we examined twelve kidney stones from ten PH I and six stones from four PH III patients. Unfortunately, no PH II stones were available for analysis. The study on this set of stones indicates a more diverse composition of PH stones than previously reported and a potential dynamic response of morphology and composition of calculi to treatment with crystallization inhibitors (citrate, magnesium) in PH I. Stones formed by PH I patients under treatment are more compact and…

MaleBiomineralizationMineral Metabolism and the KidneyAnatomy and Physiology030232 urology & nephrologyCalcium oxalatelcsh:Medicine030204 cardiovascular system & hematologyPrimary hyperoxaluriachemistry.chemical_compound0302 clinical medicineMaterials ChemistryKidney StonesStone compositionChildlcsh:ScienceMineralsMultidisciplinaryMineralogyResponse to treatmentNephrologyMedicineMaterials CharacterizationResearch ArticleBiotechnologyAdultmedicine.medical_specialtyAdolescentUrologyUrinary systemMaterials ScienceUrologyengineering.materialBiomaterialsKidney CalculiYoung Adult03 medical and health sciencesmedicineHumansBiologyCalcium OxalateWhewellitelcsh:Rmedicine.diseaseSurgerychemistryHyperoxaluria PrimaryEarth Sciencesengineeringlcsh:QKidney stonesPhysiological ProcessesWeddellitePLoS ONE
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Genome-wide association scan of quantitative traits for attention deficit hyperactivity disorder identifies novel associations and confirms candidate…

2008

Contains fulltext : 70192.pdf (Publisher’s version ) (Closed access) Attention deficit hyperactivity disorder (ADHD) is a complex condition with environmental and genetic etiologies. Up to this point, research has identified genetic associations with candidate genes from known biological pathways. In order to identify novel ADHD susceptibility genes, 600,000 SNPs were genotyped in 958 ADHD proband-parent trios. After applying data cleaning procedures we examined 429,981 autosomal SNPs in 909 family trios. We generated six quantitative phenotypes from 18 ADHD symptoms to be used in genome-wide association analyses. With the PBAT screening algorithm, we identified 2 SNPs, rs6565113 and rs5526…

MaleCandidate geneGenetics and epigenetic pathways of disease [NCMLS 6]2804 Cellular and Molecular NeuroscienceMedizinGenome-wide association studyNeuroinformatics [DCN 3]Genome2738 Psychiatry and Mental Health0302 clinical medicinePerception and Action [DCN 1]Cluster AnalysisGenetics(clinical)Genetics (clinical)Genetics0303 health sciences10058 Department of Child and Adolescent PsychiatryCadherinsPedigreePsychiatry and Mental healthFemaleFunctional Neurogenomics [DCN 2]CDH13AlgorithmsGenetic Markers2716 Genetics (clinical)GenotypeQuantitative Trait Loci610 Medicine & healthSingle-nucleotide polymorphismBiologyQuantitative trait locusPolymorphism Single NucleotideMental health [NCEBP 9]Genetic determinismGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCellular and Molecular NeuroscienceCognitive neurosciences [UMCN 3.2]medicineADHDAttention deficit hyperactivity disorderHumansGenetic Predisposition to Diseaseddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersGene030304 developmental biologyProbabilityModels GeneticGenome Humancandidate genefamily-based associationmedicine.diseaseIntronsHaplotypesGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with Hyperactivitygenome-wide association030217 neurology & neurosurgeryGenome-Wide Association StudyAmerican Journal of Medical Genetics Part B: Neuropsychiatric Genetics
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Genome-wide association scan of the time to onset of attention deficit hyperactivity disorder.

2008

Contains fulltext : 70149.pdf (Publisher’s version ) (Closed access) A time-to-onset analysis for family-based samples was performed on the genomewide association (GWAS) data for attention deficit hyperactivity disorder (ADHD) to determine if associations exist with the age at onset of ADHD. The initial dataset consisted of 958 parent-offspring trios that were genotyped on the Perlegen 600,000 SNP array. After data cleaning procedures, 429,981 autosomal SNPs and 930 parent-offspring trios were used found suitable for use and a family-based logrank analysis was performed using that age at first ADHD symptoms as the quantitative trait of interest. No SNP achieved genome-wide significance, and…

MaleCandidate geneGenetics and epigenetic pathways of disease [NCMLS 6]2804 Cellular and Molecular NeuroscienceMedizinGenome-wide association studyNeuroinformatics [DCN 3]Linkage Disequilibrium2738 Psychiatry and Mental Health0302 clinical medicinePerception and Action [DCN 1]Genetics(clinical)Age of OnsetChildGenetics (clinical)Genetics0303 health sciences10058 Department of Child and Adolescent PsychiatryPedigreePsychiatry and Mental healthChild PreschoolFemaleFunctional Neurogenomics [DCN 2]SNP arrayGenetic Markers2716 Genetics (clinical)Sodium-Hydrogen ExchangersAdolescentQuantitative Trait Loci610 Medicine & healthSingle-nucleotide polymorphismBiologyQuantitative trait locusMental health [NCEBP 9]Polymorphism Single NucleotideArticleGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCellular and Molecular NeuroscienceCognitive neurosciences [UMCN 3.2]medicineAttention deficit hyperactivity disorderSNPHumansGenetic Predisposition to Diseaseddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und Jugendalters030304 developmental biologyProbabilityRetrospective StudiesGenome Humanmedicine.diseaseGenetic defects of metabolism [UMCN 5.1]HaplotypesAttention Deficit Disorder with HyperactivityAge of onset030217 neurology & neurosurgeryGenome-Wide Association Study
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Mutations in LCA5, encoding the ciliary protein lebercilin, cause Leber congenital amaurosis

2007

Contains fulltext : 53618.pdf (Publisher’s version ) (Closed access) Leber congenital amaurosis (LCA) causes blindness or severe visual impairment at or within a few months of birth. Here we show, using homozygosity mapping, that the LCA5 gene on chromosome 6q14, which encodes the previously unknown ciliary protein lebercilin, is associated with this disease. We detected homozygous nonsense and frameshift mutations in LCA5 in five families affected with LCA. In a sixth family, the LCA5 transcript was completely absent. LCA5 is expressed widely throughout development, although the phenotype in affected individuals is limited to the eye. Lebercilin localizes to the connecting cilia of photore…

MaleCandidate geneGenetics and epigenetic pathways of disease [NCMLS 6]genetic structuresMolecular Sequence DataOptic Atrophy Hereditary LeberNeuroinformatics [DCN 3]Biologymedicine.disease_causeCiliopathiesJoubert syndromeCell LineFrameshift mutationGenomic disorders and inherited multi-system disorders [IGMD 3]MiceTranslational research [ONCOL 3]Chlorocebus aethiopsPerception and Action [DCN 1]GeneticsmedicineNeurosensory disorders [UMCN 3.3]AnimalsHumansCiliaRats WistarEye ProteinsFrameshift MutationRenal disorder [IGMD 9]GeneticsMutationCiliumDisease gene identificationmedicine.diseasePhenotypeeye diseasesPedigreeRatsMice Inbred C57BLGenetic defects of metabolism [UMCN 5.1]Codon NonsenseCOS CellsFemalesense organsFunctional Neurogenomics [DCN 2]Microtubule-Associated ProteinsNature Genetics
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A high-density SNP linkage scan with 142 combined subtype ADHD sib pairs identifies linkage regions on chromosomes 9 and 16

2008

As part of the International Multi-centre ADHD Gene (IMAGE) project we have completed an affected sibling pair study of 142 narrowly defined DSM-IV combined type ADHD proband-sibling pairs. We found suggestive linkage on chromosomes 9 and 16 with non-parametric multipoint peak LOD scores of 2.13 and 3.1 respectively. There have been several previous ADHD linkage scans. The UCLA study (Fisher et al. 2002; Ogdie et al. 2004; Ogdie et al. 2003), the Dutch study (Bakker et al. 2003), the German study (Hebebrand et al. 2006) and the MGH Study (Faraone et al., submitted) applied the affected sib pair (ASP) strategy; the Columbian study used extended pedigrees ascertained from a population isolate…

MaleGenetics and epigenetic pathways of disease [NCMLS 6]GENOMEWIDE SCANMedizin2804 Cellular and Molecular NeuroscienceCHILDRENComorbidityNeuroinformatics [DCN 3]Severity of Illness IndexDevelopmental psychology2738 Psychiatry and Mental Health0302 clinical medicinePerception and Action [DCN 1]HETEROGENEITYIsraelChildGeneticsObserver Variation0303 health sciencesATTENTION-DEFICIT/HYPERACTIVITY DISORDERPSYCHIATRIC-DISORDERSDOPAMINE TRANSPORTER GENEASSOCIATION10058 Department of Child and Adolescent PsychiatryEuropePsychiatry and Mental healthFemalePsychologyChromosomes Human Pair 9linkageFunctional Neurogenomics [DCN 2]GenotypeDEFICIT HYPERACTIVITY DISORDER610 Medicine & healthPolymorphism Single NucleotideMental health [NCEBP 9]Genetic determinismWhite PeopleGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCellular and Molecular NeuroscienceCognitive neurosciences [UMCN 3.2]Genetic linkage1312 Molecular BiologymedicineSNPAttention deficit hyperactivity disorderHumansADHDSiblingMolecular Biology030304 developmental biologyLinkage (software)SiblingsChromosomemedicine.diseaseSib pairsUnited Statesaffected sib pairsGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with HyperactivityCONDUCT DISORDERLod ScoreDISEQUILIBRIUM030217 neurology & neurosurgeryChromosomes Human Pair 16
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