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

showing 10 items of 123 documents

Opposing Effects of CREBBP Mutations Govern the Phenotype of Rubinstein-Taybi Syndrome and Adult SHH Medulloblastoma

2018

Recurrent mutations in chromatin modifiers are specifically prevalent in adolescent or adult patients with Sonic hedgehog-associated medulloblastoma (SHH MB). Here, we report that mutations in the acetyltransferase CREBBP have opposing effects during the development of the cerebellum, the primary site of origin of SHH MB. Our data reveal that loss of Crebbp in cerebellar granule neuron progenitors (GNPs) during embryonic development of mice compromises GNP development, in part by downregulation of brain-derived neurotrophic factor (Bdnf). Interestingly, concomitant cerebellar hypoplasia was also observed in patients with Rubinstein-Taybi syndrome, a congenital disorder caused by germline mu…

0301 basic medicineCerebellumCrebbp protein mousemetabolism [Cerebellar Neoplasms]acetyltransferase; cerebellum; CREBBP; development; Rubinstein-Taybi syndrome; SHH medulloblastomagenetics [Hedgehog Proteins]MiceNeurotrophic factorsmetabolism [CREB-Binding Protein]Mice KnockoutNeuronsRubinstein-Taybi Syndromepathology [Rubinstein-Taybi Syndrome]CREBBPCREB-Binding ProteinPhenotypegenetics [CREB-Binding Protein]3. Good healthpathology [Cerebellar Neoplasms]acetyltransferasePhenotypemedicine.anatomical_structuregenetics [Rubinstein-Taybi Syndrome]Femalemetabolism [Hedgehog Proteins]Signal TransductionSHH medulloblastomaAdultcerebellumBiologyGeneral Biochemistry Genetics and Molecular BiologyCREBBP; Rubinstein-Taybi syndrome; SHH medulloblastoma; acetyltransferase; cerebellum; development.03 medical and health sciencesGermline mutationAcetyltransferasesmetabolism [Medulloblastoma]medicineAnimalsHumansgenetics [Cerebellar Neoplasms]Hedgehog Proteinsddc:610Cerebellar NeoplasmsdevelopmentMolecular BiologyMedulloblastomaRubinstein–Taybi syndromegenetics [Medulloblastoma]metabolism [Rubinstein-Taybi Syndrome]pathology [Medulloblastoma]Cell Biologymedicine.disease030104 developmental biologyMutationphysiology [CREB-Binding Protein]Cancer researchSHH protein humanCerebellar hypoplasia (non-human)metabolism [Acetyltransferases]CREBBP protein humanMedulloblastomaDevelopmental BiologyCongenital disorderDevelopmental Cell
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Usher syndrome: molecular links of pathogenesis, proteins and pathways.

2006

Contains fulltext : 50437.pdf (Publisher’s version ) (Closed access) Usher syndrome is the most common form of deaf-blindness. The syndrome is both clinically and genetically heterogeneous, and to date, eight causative genes have been identified. The proteins encoded by these genes are part of a dynamic protein complex that is present in hair cells of the inner ear and in photoreceptor cells of the retina. The localization of the Usher proteins and the phenotype in animal models indicate that the Usher protein complex is essential in the morphogenesis of the stereocilia bundle in hair cells and in the calycal processes of photoreceptor cells. In addition, the Usher proteins are important in…

Genetics and epigenetic pathways of disease [NCMLS 6]Usher syndromeCell Cycle ProteinsNerve Tissue ProteinsBiologyRetinaAdherens junctionMiceHair Cells AuditoryCell polarityGeneticsmedicineotorhinolaryngologic diseasesNeurosensory disorders [UMCN 3.3]AnimalsHumansProtein IsoformsCell Cycle ProteinMolecular BiologyGenetics (clinical)Renal disorder [IGMD 9]Adaptor Proteins Signal TransducingStereociliumMembrane ProteinsSignal transducing adaptor proteinGeneral MedicineActin cytoskeletonmedicine.diseaseeye diseasesCell biologyCytoskeletal ProteinsGenetic defects of metabolism [UMCN 5.1]Ear InnerMultiprotein ComplexesCateninSynapsessense organsUsher SyndromesPhotoreceptor Cells Vertebrate
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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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A multi-centre clinico-genetic analysis of the VPS35 gene in Parkinson disease indicates reduced penetrance for disease-associated variants

2012

Abstract: Background Two recent studies identified a mutation (p.Asp620Asn) in the vacuolar protein sorting 35 gene as a cause for an autosomal dominant form of Parkinson disease. Although additional missense variants were described, their pathogenic role yet remains inconclusive. Methods and results We performed the largest multi-center study to ascertain the frequency and pathogenicity of the reported vacuolar protein sorting 35 gene variants in more than 15,000 individuals worldwide. p.Asp620Asn was detected in 5 familial and 2 sporadic PD cases and not in healthy controls, p.Leu774Met in 6 cases and 1 control, p.Gly51Ser in 3 cases and 2 controls. Overall analyses did not reveal any sig…

MaleParkinson's diseasePopulationVesicular Transport ProteinsLocus (genetics)DiseaseBiologyVPS35 protein humanBioinformaticsgenetics [Vesicular Transport Proteins]genetics [Parkinson Disease]Risk Factorsmedicinemetabolism [Vesicular Transport Proteins]GeneticsMissense mutationVPS35 GeneHumansGenetic epidemiologyGenetic Predisposition to Diseaseddc:6101506Genome-wideeducationGenetics (clinical)Genetic Association StudiesGeneticsVacuolar protein sortingeducation.field_of_studyGenotype-Phenotype CorrelationsParkinson DiseaseComplex traitsmedicine.diseasePenetranceddc:MutationFemaleHuman medicineParkinson-s diseaseJournal of Medical Genetics
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Population differences in the International Multi-Centre ADHD Gene Project.

2008

Contains fulltext : 71443.pdf (Publisher’s version ) (Closed access) The International Multi-Centre ADHD Gene sample consists of 674 families from eight countries (Belgium, England, Germany, Holland, Ireland, Israel, Spain, and Switzerland) ascertained from clinics for combined-type attention definity hyperactivity disorder in an offspring. 863 SNPs were successfully genotyped across 47 autosomal genes implicated in psychiatric disorders yielding a single nucleotide polymorphism (SNP) density of approximately one SNP per 2.5 kb. A global test of heterogeneity showed 269 SNPs nominally significant (expected 43). Inclusion of the Israeli population accounted for approximately 70% of these nom…

MaleLinkage disequilibriumInternationalityGenetics and epigenetic pathways of disease [NCMLS 6]EpidemiologyMedizinNeuroinformatics [DCN 3]Linkage Disequilibrium0302 clinical medicineGene FrequencyPerception and Action [DCN 1]International HapMap ProjectIsraelChildGenetics (clinical)0303 health scienceseducation.field_of_studyChromosome MappingSDG 10 - Reduced Inequalities10058 Department of Child and Adolescent PsychiatryGeographyChild Preschool/dk/atira/pure/sustainabledevelopmentgoals/reduced_inequalitiesFemaleFunctional Neurogenomics [DCN 2]Genetic Markers2716 Genetics (clinical)AdolescentPopulationSample (statistics)Single-nucleotide polymorphism610 Medicine & healthMental health [NCEBP 9]Polymorphism Single NucleotideWhite PeopleGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCognitive neurosciences [UMCN 3.2]SNPHumansddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendalterseducationGene030304 developmental biologyGenetic VariationGenetics PopulationGenetic defects of metabolism [UMCN 5.1]HaplotypesSample size determinationAttention Deficit Disorder with Hyperactivity030217 neurology & neurosurgeryDemography2713 Epidemiology
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New insights in the neurological phenotype of aceruloplasminemia in Caucasian patients

2017

Abstract Introduction The diagnosis aceruloplasminemia is usually made in patients with advanced neurological manifestations of the disease. In these patients prognosis is poor, disabilities are severe and patients often die young. The aim of our study was to facilitate recognition of aceruloplasminemia at a disease stage at which treatment can positively influence outcome. Currently, the neurological phenotype of aceruloplasminemia has been mainly described in Japanese patients. This ‘classical’ phenotype consists of cerebellar ataxia, hyperkinetic movement disorders and cognitive decline. In this study we describe the spectrum of neurological disease in Caucasian patients. Methods Data on…

0301 basic medicineAdultMalemedicine.medical_specialtyPediatricsAtaxiaMovement disordersBiologyWhite People03 medical and health sciencesNeurological manifestation0302 clinical medicinePhenotypic variabilitymedicineAceruloplasminemiaHumansCognitive declineAceruloplasminemiaPsychiatryDystoniaCerebellar ataxiaParkinsonismCeruloplasminChoreaNeurodegenerative DiseasesMiddle Agedmedicine.diseaseIron Metabolism DisordersPedigree030104 developmental biologyPsychiatric changesPhenotypeNeurologyFemaleNeurology (clinical)Geriatrics and Gerontologymedicine.symptomNervous System DiseasesSettore M-EDF/01 - Metodi E Didattiche Delle Attivita' Motorie030217 neurology & neurosurgeryFollow-Up Studies
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Patients' and physicians' preferences for type 2 diabetes mellitus treatments in Spain and Portugal: a discrete choice experiment.

2015

Objective: To assess Spanish and Portuguese patients' and physicians' preferences regarding type 2 diabetes mellitus (T2DM) treatments and the monthly willingness to pay (WTP) to gain benefits or avoid side effects. Methods: An observational, multicenter, exploratory study focused on routine clinical practice in Spain and Portugal. Physicians were recruited from multiple hospitals and outpatient clinics, while patients were recruited from eleven centers operating in the public health care system in different autonomous communities in Spain and Portugal. Preferences were measured via a discrete choice experiment by rating multiple T2DM medication attributes. Data were analyzed using the cond…

:Geographicals::Geographic Locations::Europe::Portugal [Medical Subject Headings]cardiovascular riskHbA1cendocrine system diseases:Analytical Diagnostic and Therapeutic Techniques and Equipment::Diagnosis::Diagnostic Techniques and Procedures::Physical Examination::Body Constitution::Body Weights and Measures::Body Mass Index [Medical Subject Headings]:Diseases::Nutritional and Metabolic Diseases::Metabolic Diseases::Glucose Metabolism Disorders::Hypoglycemia [Medical Subject Headings]:Disciplines and Occupations::Health Occupations::Medicine::Public Health [Medical Subject Headings]:Analytical Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Statistics as Topic::Probability::Risk::Risk Factors [Medical Subject Headings]:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings]:Named Groups::Persons::Occupational Groups::Health Personnel::Physicians [Medical Subject Headings]HbA(1c)HbA:Diseases::Pathological Conditions Signs and Symptoms::Signs and Symptoms::Body Weight::Body Weight Changes::Weight Loss [Medical Subject Headings]:Diseases::Cardiovascular Diseases [Medical Subject Headings]preferences:Geographicals::Geographic Locations::Europe::Spain [Medical Subject Headings]diabetesnutritional and metabolic diseasesPeso corporalweightPérdida de peso:Health Care::Health Care Facilities Manpower and Services::Health Facilities::Ambulatory Care Facilities [Medical Subject Headings]Diabetes mellitus tipo 2:Diseases::Pathological Conditions Signs and Symptoms::Signs and Symptoms::Signs and Symptoms Digestive::Nausea [Medical Subject Headings]hypoglycemia:Analytical Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Statistics as Topic::Models Statistical::Logistic Models [Medical Subject Headings]:Diseases::Pathological Conditions Signs and Symptoms::Signs and Symptoms::Body Weight [Medical Subject Headings]:Diseases::Nutritional and Metabolic Diseases::Metabolic Diseases::Glucose Metabolism Disorders::Diabetes Mellitus::Diabetes Mellitus Type 2 [Medical Subject Headings]:Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Physiological Effects of Drugs::Hypoglycemic Agents [Medical Subject Headings]Enfermedades cardiovascularesHipoglucemiawillingness to pay:Check Tags [Medical Subject Headings]discrete choice model
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DSM-IV Combined Type ADHD Shows Familial Association With Sibling Trait Scores

2008

Contains fulltext : 69060.pdf (Publisher’s version ) (Closed access) Attention deficit hyperactivity disorder (ADHD) is a discrete clinical syndrome characterized by the triad of inattention, hyperactivity, and impulsivity in the context of marked impairments. Molecular genetic studies have been successful in identifying genetic variants associated with ADHD, particularly with DSM-IV inattentive and combined subtypes. Quantitative trait locus (QTL) approaches to linkage and association mapping have yet to be widely used in ADHD research, although twin studies investigating individual differences suggest that genetic liability for ADHD is continuously distributed throughout the population, u…

Malequantitative geneticsGenetics and epigenetic pathways of disease [NCMLS 6]Genetic Linkageattention deficit hyperactivity disorder (ADHD)GENOMEWIDE SCANMedizin2804 Cellular and Molecular NeuroscienceNeuroinformatics [DCN 3]MULTIPLE-REGRESSION ANALYSIS2738 Psychiatry and Mental Health0302 clinical medicineDIFFICULTIES QUESTIONNAIREDEFICIT-HYPERACTIVITY DISORDERTwins DizygoticPerception and Action [DCN 1]Genetics(clinical)DF analysisAssociation mappingGenetics (clinical)linkage studyGeneticseducation.field_of_studyATTENTION-DEFICIT/HYPERACTIVITY DISORDERDOPAMINE TRANSPORTER GENE10058 Department of Child and Adolescent PsychiatryDiagnostic and Statistical Manual of Mental DisordersPsychiatry and Mental healthCHILD-BEHAVIOR CHECKLISTConduct disorderRegression AnalysisFemalemedicine.symptomFunctional Neurogenomics [DCN 2]Clinical psychology2716 Genetics (clinical)Quantitative Trait LociPopulation610 Medicine & healthQuantitative trait locusBiologyImpulsivityMental health [NCEBP 9]behavioral disciplines and activitiesINDIVIDUAL-DIFFERENCESInterviews as TopicGenomic disorders and inherited multi-system disorders [IGMD 3]quantitative trait locus (QTL)03 medical and health sciencesCellular and Molecular NeuroscienceCognitive neurosciences [UMCN 3.2]mental disordersmedicineHumansSibling RelationsAttention deficit hyperactivity disorderFamilyGenetic Predisposition to Diseaseddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersSiblingeducationTWIN DATAmedicine.diseaseTwin study030227 psychiatryGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with HyperactivityCONDUCT DISORDER030217 neurology & neurosurgeryAmerican Journal of Medical Genetics. Part B: Neuropsychiatric Genetics
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Autism and carnitine: A possible link

2019

Patients with autism spectrum disorders (ASD) present deficits in social interactions and communication, they also show limited and stereotypical patterns of behaviors and interests. The pathophysiological bases of ASD have not been defined yet. Many factors seem to be involved in the onset of this disorder. These include genetic and environmental factors, but autism is not linked to a single origin, only. Autism onset can be connected with various factors such as metabolic disorders: including carnitine deficiency. Carnitine is a derivative of two amino acid lysine and methionine. Carnitine is a cofactor for a large family of enzymes: the carnitine acyltransferases. Through their action th…

0301 basic medicineAutismMetabolic homeostasisBioinformatics03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCarnitinemental disordersmedicineDietary supplementationCarnitineMethioninebusiness.industryCarnitine AcyltransferasesMinireviewsmedicine.diseaseMetabolism disorderMetabolism030104 developmental biologychemistry030220 oncology & carcinogenesisPathophysiological basesNeurodevelopmentalAutismbusinessmedicine.drugWorld Journal of Biological Chemistry
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Faim2 contributes to neuroprotection by erythropoietin in transient brain ischemia.

2018

Delayed cell death in the penumbra region of acute ischemic stroke occurs through apoptotic mechanisms, making it amenable to therapeutic interventions. Fas/CD95 mediates apoptotic cell death in response to external stimuli. In mature neurons, Fas/CD95 signaling is modulated by Fas-apoptotic inhibitory molecule 2 (Faim2), which reduces cell death in animal models of stroke, meningitis, and Parkinson disease. Erythropoietin (EPO) has been studied as a therapeutic strategy in ischemic stroke. Erythropoietin stimulates the phosphatidylinositol-3 kinase/Akt (PI3K/Akt) pathway, which regulates Faim2 expression. Therefore, up-regulation of Faim2 may contribute to neuroprotection by EPO. Male Faim…

Male0301 basic medicinemetabolism [Apoptosis Regulatory Proteins]FAIM2 protein humanlifeguard protein mouseIschemiaNerve Tissue Proteinspathology [Ischemic Attack Transient]physiology [Neuroprotection]PharmacologyBiochemistryNeuroprotectionmetabolism [Erythropoietin]metabolism [Ischemic Attack Transient]Brain ischemiaMice03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinemedicineAnimalsHumansddc:610ErythropoietinStrokeProtein kinase BPI3K/AKT/mTOR pathwayAgedpharmacology [Erythropoietin]Mice Knockoutmetabolism [Nerve Tissue Proteins]business.industryPenumbraMembrane ProteinsMiddle Agedmedicine.diseaseNeuroprotection030104 developmental biologyIschemic Attack TransientErythropoietinphysiopathology [Ischemic Attack Transient]FemaleDose-dependency ; Erythropoietin ; Fas-apoptotic Inhibitory Molecule 2 ; Ischemia-reperfusion ; Neuroprotection ; StrokeApoptosis Regulatory Proteinsbusinessmetabolism [Membrane Proteins]030217 neurology & neurosurgerymedicine.drug
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