Search results for "Frames"

showing 10 items of 265 documents

Influence of column shear failure on pushover based assessment of masonry infilled reinforced concrete framed structures: A case study

2017

Structural frames, constructed either of steel or reinforced concrete (RC), are often infilled with masonry panels. However, during the analysis of the structural frames, it has become common practice to disregard the existence of infills because of the complexity in modeling. This omission should not be allowed because the two contributions (of infills and of frames) complement each other in providing a so different structural system. The use of different modeling assumptions significantly affects the capacity as well as the inelastic demand and safety assessment. In specific, the adoption of equivalent diagonal pin-jointed struts leaves open the problem of the evaluation of the additional…

Local shear action; Masonry infill wall panels; Pushover analysis; RC frames; Civil and Structural Engineering; Geotechnical Engineering and Engineering Geology; Soil ScienceEngineeringDiagonalStructural system0211 other engineering and technologiesRC frameSoil Science020101 civil engineering02 engineering and technology0201 civil engineeringGeotechnical engineeringLocal shear actionRC framesMasonry infill wall panelsCivil and Structural Engineering021110 strategic defence & security studiesbusiness.industryMasonry infill wall panelRc framesStructural engineeringMasonryReinforced concreteGeotechnical Engineering and Engineering GeologyShear (geology)Pushover analysiAxial forcebusinessPushover analysis
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MICROSCOPIC TECHNIQUES (SEM AND OM) AND ANALYTICAL APPROACH TO CHARACTERIZE CONSTITUTIVE MATERIALS AND TECHNIQUE OF THE WOODEN FRAMES IN SICILY

2015

Nowadays artworks traditionally included in the category of applied or decorative arts are considered at the same level of fine arts getting over the old definition of minor art. According to this consideration an increasing number of studies and paper deals with the decorative arts and the Observatory for Decorative Arts in Italy “Maria Accascina” (OADI) was settled within the University of Palermo in order to study them. Nevertheless most studies deal with artistic and historic issues of applied arts and just few concern with the technique used, at least in the southern part of Italy. This paper is a systematic research concerning the constitutive materials and the executive techniques of…

MICROSCOPIC TECHNIQUES SEM OM WOODEN FRAMESSettore ING-IND/22 - Scienza E Tecnologia Dei Materiali
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Mutation profile of the MYO7A gene in Spanish patients with Usher syndrome type I.

2006

Usher syndrome type I is the most severe form of Usher syndrome. It is an autosomal recessive disorder characterized by profound congenital sensorineural deafness, retinitis pigmentosa, and vestibular abnormalities. Mutations in the myosin VIIA gene (MYO7A) are responsible for Usher syndrome type 1B (USH1B). This gene is thought to bear greatest responsibility for USH1 and, depending on the study, has been reported to account for between 24% and 59% of USH1 cases. In this report a mutation screening of the MYO7A gene was carried out in a series of 48 unrelated USH1 families using single strand conformation polymorphism analysis (SSCP) and direct sequencing of those fragments showed an abnor…

MYO7AUsher syndromeDNA Mutational AnalysisBiologyMyosinsFrameshift mutationRetinitis pigmentosaotorhinolaryngologic diseasesGeneticsmedicineMissense mutationHumansGenetic Predisposition to DiseaseGeneGenetics (clinical)Polymorphism Single-Stranded ConformationalGeneticsPolymorphism GeneticModels GeneticDyneinsSingle-strand conformation polymorphismmedicine.diseaseeye diseasesStop codonGene Expression RegulationSpainMyosin VIIaMutationUsher SyndromesHuman mutation
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Bainbridge-Ropers syndrome caused by loss-of-function variants in ASXL3: a recognizable condition

2016

International audience; Truncating ASXL3 mutations were first identified in 2013 by Bainbridge et al. as a cause of syndromic intellectual disability in four children with similar phenotypes using whole-exome sequencing. The clinical features - postulated by Bainbridge et al. to be overlapping with Bohring-Opitz syndrome - were developmental delay, severe feeding difficulties, failure to thrive and neurological abnormalities. This condition was included in OMIM as 'Bainbridge-Ropers syndrome' (BRPS, #615485). To date, a total of nine individuals with BRPS have been published in the literature in four reports (Bainbridge et al., Dinwiddie et al, Srivastava et al. and Hori et al.). In this re…

Male0301 basic medicinemedicine.medical_specialtyMicrocephalyfamilyAdolescentphenotypeDevelopmental DisabilitiesSevere muscular hypotoniaMedizinTrigonocephaly030105 genetics & heredityBiologyArticle03 medical and health sciencesIntellectual disabilityGeneticsmedicineHumansCraniofacial[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsnovo frameshift mutationgenedisordersGenetics (clinical)GeneticsInfantSyndromemedicine.diseaseDermatologyFailure to Thrive030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsintellectual disabilityChild Preschoolbohring-opitz syndromeMutationFailure to thriveMedical geneticsFemalemedicine.symptomBohring–Opitz syndromeTranscription Factors
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SPRED1, a RAS MAPK pathway inhibitor that causes Legius syndrome, is a tumour suppressor downregulated in paediatric acute myeloblastic leukaemia

2013

Constitutional dominant loss-of-function mutations in the SPRED1 gene cause a rare phenotype referred as neurofibromatosis type 1 (NF1)-like syndrome or Legius syndrome, consisted of multiple café-au-lait macules, axillary freckling, learning disabilities and macrocephaly. SPRED1 is a negative regulator of the RAS MAPK pathway and can interact with neurofibromin, the NF1 gene product. Individuals with NF1 have a higher risk of haematological malignancies. SPRED1 is highly expressed in haematopoietic cells and negatively regulates haematopoiesis. SPRED1 seemed to be a good candidate for leukaemia predisposition or transformation. We performed SPRED1 mutation screening and expression status i…

MaleCancer ResearchAdolescentLoss of HeterozygosityFrameshift mutationGene productLoss of heterozygosityPrecursor B-Cell Lymphoblastic Leukemia-Lymphomahemic and lymphatic diseasesGeneticsmedicineHumansGenes Tumor SuppressorNeurofibromatosisChildMolecular BiologyAdaptor Proteins Signal TransducingLegius syndromeNeurofibromin 1biologyCafe-au-Lait SpotsInfant NewbornIntracellular Signaling Peptides and ProteinsMacrocephalyInfantMembrane Proteinsmedicine.diseaseNeurofibromin 1Gene Expression Regulation NeoplasticLeukemia Myeloid AcuteHaematopoiesisGenes rasChild PreschoolMutationCancer researchbiology.proteinFemalemedicine.symptomOncogene
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The genomic landscape of the Ewing Sarcoma family of tumors reveals recurrent STAG2 mutation.

2014

The Ewing sarcoma family of tumors (EFT) is a group of highly malignant small round blue cell tumors occurring in children and young adults. We report here the largest genomic survey to date of 101 EFT (65 tumors and 36 cell lines). Using a combination of whole genome sequencing and targeted sequencing approaches, we discover that EFT has a very low mutational burden (0.15 mutations/Mb) but frequent deleterious mutations in the cohesin complex subunit STAG2 (21.5% tumors, 44.4% cell lines), homozygous deletion of CDKN2A (13.8% and 50%) and mutations of TP53 (6.2% and 71.9%). We additionally note an increased prevalence of the BRCA2 K3326X polymorphism in EFT patient samples (7.3%) compared …

MaleCancer ResearchCell Cycle Proteinsmedicine.disease_causeFusion geneCDKN2AMedicine and Health Sciences2.1 Biological and endogenous factorsAetiologyChildGenetics (clinical)CancerPediatricMutationTissue microarrayTumorGenomeSarcomasHigh-Throughput Nucleotide SequencingAntigens NuclearSarcomaNeoplasm ProteinsOncologyChild PreschoolFemaleSarcomaResearch ArticleBiotechnologyHumanAdultPediatric Research Initiativelcsh:QH426-470Cohesin complexAdolescentPediatric CancerEwing SarcomaSarcoma EwingBiologyDisease-Free SurvivalFrameshift mutationCell LineGermline mutationRare DiseasesCell Line TumorEwingCancer GeneticsmedicineGeneticsHumansNuclearGenetic TestingAntigensPreschoolMolecular BiologyEcology Evolution Behavior and SystematicsGenome HumanHuman GenomeBiology and Life SciencesCancers and NeoplasmsInfantmedicine.diseaselcsh:GeneticsOrphan DrugMutationCancer researchGene DeletionDevelopmental Biology
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The DYRK1A gene is a cause of syndromic intellectual disability with severe microcephaly and epilepsy.

2012

Background DYRK1A plays different functions during development, with an important role in controlling brain growth through neuronal proliferation and neurogenesis. It is expressed in a gene dosage dependent manner since dyrk1a haploinsufficiency induces a reduced brain size in mice, and DYRK1A overexpression is the candidate gene for intellectual disability (ID) and microcephaly in Down syndrome. We have identified a 69 kb deletion including the 5′ region of the DYRK1A gene in a patient with growth retardation, primary microcephaly, facial dysmorphism, seizures, ataxic gait, absent speech and ID. Because four patients previously reported with intragenic DYRK1A rearrangements or 21q22 microd…

MaleCandidate geneDown syndromeMicrocephalyAdolescentGenotypeBiologyProtein Serine-Threonine KinasesBioinformaticsFrameshift mutationEpilepsyAngelman syndromeIntellectual DisabilityGene OrderGeneticsmedicineHumansChildGenetics (clinical)GeneticsEpilepsyBase SequenceFaciesElectroencephalographySyndromeProtein-Tyrosine Kinasesmedicine.diseasePhenotypeChild PreschoolSpeech delayMutationMicrocephalyFemalemedicine.symptomHaploinsufficiencyJournal of medical genetics
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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 very mild phenotype of Charcot-Marie-Tooth disease type 4H caused by two novel mutations in FGD4

2019

Abstract Background Mutations in the FGD4 gene cause an autosomal recessive demyelinating peripheral neuropathy referred to as CMT4H, characterized by its onset in infancy or early-childhood and its slow progression. Methods The clinical and genetic status of two patients with CMT4H was studied, performing genetic testing with a panel of genes and analysing FGD4 mRNA expression by quantitative PCR. Results Two novel FGD4 variants (c.514delG and c.2211dupA) were identified in two mildly affected Spanish siblings with CMT4H, and with disease onset in late adolescence/adulthood (one of them remaining asymptomatic at 20). On examination, foot deformity was observed without weakness or sensory i…

MaleCharcot-Marie-ToothPathologymedicine.medical_specialtyAdolescentFGD4medicine.disease_causeAsymptomaticYoung Adult03 medical and health sciences0302 clinical medicineCharcot-Marie-Tooth DiseaseCharcot-Marie-Tooth disease type 4HCMT4HmedicineHumans030212 general & internal medicineAlleleFrameshift MutationGeneAllelesGenetic testingMutationmedicine.diagnostic_testbusiness.industrySiblingsCMTMicrofilament Proteinsmedicine.diseasePhenotypePedigreeNeuropathyPhenotypePeripheral neuropathyNeurologyFemaleNeurology (clinical)medicine.symptombusiness030217 neurology & neurosurgeryJournal of the Neurological Sciences
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SPG10 is a rare cause of spastic paraplegia in European families.

2008

Contains fulltext : 71099.pdf (Publisher’s version ) (Closed access) BACKGROUND: SPG10 is an autosomal dominant form of hereditary spastic paraplegia (HSP), which is caused by mutations in the neural kinesin heavy chain KIF5A gene, the neuronal motor of fast anterograde axonal transport. Only four mutations have been identified to date. OBJECTIVE: To determine the frequency of SPG10 in European families with HSP and to specify the SPG10 phenotype. PATIENTS AND METHODS: 80 index patients from families with autosomal dominant HSP were investigated for SPG10 mutations by direct sequencing of the KIF5A motor domain. Additionally, the whole gene was sequenced in 20 of these families. RESULTS: Th…

MaleDNA Mutational AnalysisKinesinsHEREDITARYmedicine.disease_cause0302 clinical medicineSpasticPerception and Action [DCN 1]Missense mutationKIF5AAge of OnsetChildFrameshift MutationMUTATIONGenes DominantGeneticsNeurologic Examination0303 health sciencesMutationSplice site mutationSITEExonsMiddle AgedAnterograde axonal transport3. Good healthPedigreeEuropePsychiatry and Mental healthPhenotypeATAXIASChild PreschoolFemaleChromosome DeletionMOTORFunctional Neurogenomics [DCN 2]AdultNeuromuscular diseaseGenotypeHereditary spastic paraplegiaMutation Missense03 medical and health sciencesCognitive neurosciences [UMCN 3.2]medicineHumansGait Disorders Neurologic030304 developmental biologyChromosome Aberrationsbusiness.industrySpastic Paraplegia HereditarySequence Analysis DNAmedicine.diseaseGENEPeripheral neuropathyGenetics PopulationSurgeryNeurology (clinical)RNA Splice Sitesbusiness030217 neurology & neurosurgeryJournal of neurology, neurosurgery, and psychiatry
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