Search results for "cml"

showing 10 items of 91 documents

Meta-analysis of genome-wide linkage scans of attention deficit hyperactivity disorder

2008

Contains fulltext : 69243.pdf (Publisher’s version ) (Closed access) Genetic contribution to the development of attention deficit hyperactivity disorder (ADHD) is well established. Seven independent genome-wide linkage scans have been performed to map loci that increase the risk for ADHD. Although significant linkage signals were identified in some of the studies, there has been limited replications between the various independent datasets. The current study gathered the results from all seven of the ADHD linkage scans and performed a Genome Scan Meta Analysis (GSMA) to identify the genomic region with most consistent linkage evidence across the studies. Genome-wide significant linkage (P(S…

Genetics and epigenetic pathways of disease [NCMLS 6]Genetic LinkageEuropean Continental Ancestry GroupMedizinGenome ScanBiologyNeuroinformatics [DCN 3]Mental health [NCEBP 9]Genetic determinismWhite PeopleArticleChromosomesGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineGene mappingCognitive neurosciences [UMCN 3.2]Genetic linkageGenetic predispositionmedicinePerception and Action [DCN 1]Attention deficit hyperactivity disorderHumansddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersGenetics (clinical)030304 developmental biologyProbabilityLinkage (software)Genetics0303 health sciencesGenomeGenome HumanPair 16Chromosome Mappingmedicine.diseasePsychiatry and Mental healthGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with HyperactivityMeta-analysisLod ScoreFunctional Neurogenomics [DCN 2]030217 neurology & neurosurgeryChromosomes Human Pair 16HumanAmerican Journal of Medical Genetics. Part B: Neuropsychiatric Genetics
researchProduct

No association between two polymorphisms of the serotonin transporter gene and combined type attention deficit hyperactivity disorder.

2008

Contains fulltext : 71091.pdf (Publisher’s version ) (Closed access) Several independent studies have reported association between serotonin transporter gene (SLC6A4) polymorphisms and attention deficit hyperactivity disorder (ADHD). Five studies found evidence for association between the long-allele of a 44-bp insertion/deletion polymorphism (5-HTTLPR) and ADHD. Another two studies corroborated this finding while a further six studies did not find such an association. For a second polymorphism within the gene, a variable number tandem repeat (VNTR) within intron 2, one study demonstrated that the 12/12 genotype was significantly less frequent in ADHD cases compared to controls, while a sec…

Genetics and epigenetic pathways of disease [NCMLS 6]MedizinNeuroinformatics [DCN 3]0302 clinical medicinePolymorphism (computer science)GenotypePerception and Action [DCN 1]Childhealth care economics and organizationsSerotonin transporterGenetics (clinical)GeneticsSerotonin Plasma Membrane Transport Proteins0303 health sciencesDepression030305 genetics & heredityTransmission disequilibrium testhumanitiesVariable number tandem repeatPsychiatry and Mental healthChild Preschool/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFunctional Neurogenomics [DCN 2]medicine.medical_specialtyAdolescenteducationBiologybehavioral disciplines and activitiesMental health [NCEBP 9]Genomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCellular and Molecular NeuroscienceSDG 3 - Good Health and Well-beingCognitive neurosciences [UMCN 3.2]Internal medicinemental disordersmedicineAttention deficit hyperactivity disorderHumansGenetic Predisposition to Diseaseddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersAssociation (psychology)Gene030304 developmental biologyFamily HealthPolymorphism Geneticbusiness.industryMood Disordersmedicine.diseaseMoodEndocrinologyMood disordersGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with Hyperactivitybiology.proteinbusiness030217 neurology & neurosurgery
researchProduct

Sequence variants of the DFNB31 gene among Usher syndrome patients of diverse origin.

2010

Contains fulltext : 89306.pdf (Publisher’s version ) (Open Access) PURPOSE: It has been demonstrated that mutations in deafness, autosomal recessive 31 (DFNB31), the gene encoding whirlin, is responsible for nonsyndromic hearing loss (NSHL; DFNB31) and Usher syndrome type II (USH2D). We screened DFNB31 in a large cohort of patients with different clinical subtypes of Usher syndrome (USH) to determine the prevalence of DFNB31 mutations among USH patients. METHODS: DFNB31 was screened in 149 USH2, 29 USH1, six atypical USH, and 11 unclassified USH patients from diverse ethnic backgrounds. Mutation detection was performed by direct sequencing of all coding exons. RESULTS: We identified 38 diff…

Genetics and epigenetic pathways of disease [NCMLS 6]MutationMutation Missenseotorhinolaryngologic diseasesGenetic VariationHumansMembrane ProteinsFunctional Neurogenomics [DCN 2]Usher SyndromesIntronseye diseasesResearch Article
researchProduct

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
researchProduct

De novo 13q deletions in two patients with mild anorectal malformations as part of VATER/VACTERL and VATER/VACTERL-like association and analysis of E…

2013

Item does not contain fulltext Anorectal malformations (ARMs) comprise a broad spectrum of conditions ranging from mild anal anomalies to complex cloacal malformations. In 40-50% of cases, ARM occurs within the context of defined genetic syndromes or complex multiple congenital anomalies, such as VATER/VACTERL (vertebral defects [V], ARMs [A], cardiac defects [C], tracheoesophageal fistula with or without esophageal atresia [TE], renal malformations [R], and limb defects [L]) association. Here, we report the identification of deletions at chromosome 13q using single nucleotide polymorphism-based array analysis in two patients with mild ARM as part of VATER/VACTERL and VATER/VACTERL-like ass…

Heart Defects CongenitalMalemedicine.medical_specialtyCandidate geneLimb Deformities CongenitalTracheoesophageal fistulaSingle-nucleotide polymorphismContext (language use)Chromosome DisordersEphrin-B2BiologyGastroenterologyAnus ImperforateMiceEsophagusInternal medicineGeneticsmedicineAnimalsHumansIn patientGenetics (clinical)Mice KnockoutChromosomes Human Pair 13Infant NewbornChromosomeAnatomymedicine.diseaseAnorectal MalformationsSpineTracheaDisease Models AnimalRadiusHuman Reproduction Renal disorder [NCEBP 12]Evaluation of complex medical interventions [NCEBP 2]AtresiaChild PreschoolMutationMutation testingFemaleChromosome DeletionGenetics and epigenetic pathways of disease Genomic disorders and inherited multi-system disorders [NCMLS 6]American Journal of Medical Genetics. Part A
researchProduct

Molecular characterization of imatinib-resistant CML cell lines by proteomic profiling

2006

Imatinib-resistanceproteomic profilingCML
researchProduct

Identification of avarol derivatives as potential antipsoriatic drugs using an in vitro model for keratinocyte growth and differentiation.

2006

Contains fulltext : 49512schalkwijk.pdf (Publisher’s version ) (Closed access) Avarol, a marine sesquiterpenoid hydroquinone, and 14 avarol derivatives have shown interesting anti-inflammatory properties in previous studies. In this study, avarol and derivatives were evaluated in high-throughput keratinocyte culture models using cytokeratin 10 and SKALP/Elafin expression as markers for respectively normal and psoriatic differentiation. Avarol and five of its derivatives (5, 10, 13, 14 and 15) were selected for further study. Only 10, 13, 14 and 15 were able to inhibit keratinocyte cell growth. Changes in expression levels of 22 genes were assessed by quantitative real time PCR (qPCR). From …

KeratinocytesDrug Evaluation PreclinicalAntineoplastic AgentsEnzyme-Linked Immunosorbent AssayIn Vitro TechniquesBiologyGeneral Biochemistry Genetics and Molecular BiologyDownregulation and upregulationTranslational research [ONCOL 3]DysideaGene expressionDithranolmedicineAnimalsHumansPsoriasisRNA MessengerGeneral Pharmacology Toxicology and PharmaceuticsCells CulturedCell ProliferationChronic inflammation and autoimmunity [UMCN 4.2]Messenger RNATumor Necrosis Factor-alphaCell growthInterleukin-8Membrane ProteinsCell DifferentiationGeneral MedicineMolecular biologyElafinPathogenesis and modulation of inflammation [N4i 1]medicine.anatomical_structureMechanism of actionCyclooxygenase 2KeratinsClinical Pharmacology and physiology [CTR 2]medicine.symptomKeratinocyteSesquiterpenesInfection and autoimmunity [NCMLS 1]Elafinmedicine.drug
researchProduct

Association of ADHD with genetic variants in the 5'-region of the dopamine transporter gene: evidence for allelic heterogeneity.

2008

Contains fulltext : 69953.pdf (Publisher’s version ) (Closed access) Multiple studies have reported an association between attention deficit hyperactivity disorder (ADHD) and the 10-repeat allele of a variable number tandem repeat (VNTR) polymorphism in the 3'-untranslated region (3'UTR) of the dopamine transporter gene (DAT1). Yet, recent meta-analyses of available data find little or no evidence for this association; although there is strong evidence for heterogeneity between datasets. This pattern of findings could arise for several reasons including the presence of relatively rare risk alleles on common haplotype backgrounds or the functional interaction of two or more loci within the g…

Linkage disequilibriumGenetics and epigenetic pathways of disease [NCMLS 6]Medizin2804 Cellular and Molecular NeuroscienceNeuroinformatics [DCN 3]Linkage Disequilibrium2738 Psychiatry and Mental Health0302 clinical medicineGene FrequencyRisk FactorsPerception and Action [DCN 1]Genetics(clinical)Promoter Regions GeneticGenetics (clinical)Genetics0303 health sciences10058 Department of Child and Adolescent PsychiatryEuropeVariable number tandem repeatPsychiatry and Mental health/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingAllelic heterogeneityFunctional Neurogenomics [DCN 2]Genetic Markers2716 Genetics (clinical)Single-nucleotide polymorphism610 Medicine & healthBiologyPolymorphism Single NucleotideMental health [NCEBP 9]White PeopleGenomic disorders and inherited multi-system disorders [IGMD 3]Genetic Heterogeneity03 medical and health sciencesCellular and Molecular NeuroscienceSDG 3 - Good Health and Well-beingCognitive neurosciences [UMCN 3.2]Humansddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersAlleleAllele frequencyAlleles030304 developmental biologyDopamine Plasma Membrane Transport ProteinsGenetic heterogeneityHaplotypeGenetic VariationHaplotypesGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with Hyperactivity5' Untranslated Regions030217 neurology & neurosurgeryMicrosatellite Repeats
researchProduct

Tiratricol neutralizes bacterial endotoxins and reduces lipopolysaccharide-induced TNF-alpha production in the cell.

2008

Contains fulltext : 70610.pdf (Publisher’s version ) (Closed access) The screening of a commercially available library of compounds has proved a successful strategy for the identification of a lead compound in a drug discovery programme. Here, we analysed 880 off-patent drugs, which initially comprised the Prestwick Chemical library, as sources of bacterial endotoxin neutralizers. We identified 3,3',5-triiodo-thyroacetic acid (tiratricol) as a non-antibacterial compound that neutralizes the toxic lipopolysaccharide.

LipopolysaccharidesendotoxinLipopolysaccharideCelllipopolysaccharide-antagonistsBiology:Enginyeria dels materials [Àrees temàtiques de la UPC]BiochemistryCell LineChemical libraryMicrobiologyLipid ASepsissepsisMiceStructure-Activity Relationshipchemistry.chemical_compoundtumour necrosis factor-alphaDrug DiscoveryEscherichia colimedicineAnimalsDrugs--Designlipid APharmacologyTriiodothyroacetic acidMedicaments -- DissenyTumor Necrosis Factor-alphaDrug discoveryOrganic Chemistrylipopolysaccharidetumour necrosis factor-amedicine.diseaseAnti-Bacterial AgentsEndotoxinsmedicine.anatomical_structurechemistryTriiodothyronineMolecular Medicineseptic shockLead compoundImmunity infection and tissue repair [NCMLS 1]
researchProduct

Power-aware design of MCML logarithmic adders

2010

This paper describes the low-power design of a MOS current-mode logarithmic adder. The adder utilizes the Brent-Kung tree structure. The design strategy adopted is very simple and effective. Moreover, it can be utilized also for other types of logarithmic adders. To validate it, several adders were designed in a TSMC CMOS 130nm technology. Results of simulations indicate that the proposed methodology offers a good starting point before fine-tuning the design by SPICE simulations. Finally, the tradeoff that can be realized between performance and power consumption is discussed.

MOS current-mode logic MCML logarithmic adders Brent-Kung tree structureSettore ING-INF/01 - Elettronica
researchProduct