Search results for "EXPA"

showing 10 items of 820 documents

Phosphorus-Chalcogen Ring Expansion and Metal Coordination

2017

The reactivity of 4-membered (RPCh)2 rings (Ch = S, Se) that contain phosphorus in the +3 oxidation state is reported. These compounds undergo ring expansion to (RPCh)3 with the addition of a Lewis base. The 6-membered rings were found to be more stable than the 4-membered precursors, and the mechanism of their formation was investigated experimentally and by density functional theory calculations. The computational work identified two plausible mechanisms involving a phosphinidene chalcogenide intermediate, either as a free species or stabilized by a suitable base. Both the 4- and 6-membered rings were found to react with coinage metals, giving the same products: (RPCh)3 rings bound to the…

metal coordination010405 organic chemistryChemistryInorganic chemistryCoinage metals010402 general chemistryRing (chemistry)01 natural sciences0104 chemical sciencesInorganic ChemistryMetalCrystallographyChalcogenring expansionOxidation statePhosphinidenevisual_artvisual_art.visual_art_mediumReactivity (chemistry)Lewis acids and basesPhysical and Theoretical Chemistryphosphorus-chalcogenta116
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Global representation and multiscale expansion for the Dirichlet problem in a domain with a small hole close to the boundary

2019

For each pair (Formula presented.) of positive parameters, we define a perforated domain (Formula presented.) by making a small hole of size (Formula presented.) in an open regular subset (Formula presented.) of (Formula presented.) ((Formula presented.)). The hole is situated at distance (Formula presented.) from the outer boundary (Formula presented.) of the domain. Thus, when (Formula presented.) both the size of the hole and its distance from (Formula presented.) tend to zero, but the size shrinks faster than the distance. Next, we consider a Dirichlet problem for the Laplace equation in the perforated domain (Formula presented.) and we denote its solution by (Formula presented.) Our ai…

multiscale asymptotic expansionmulti-scale asymptotic expansionBoundary (topology)01 natural sciences35J25; 31B10; 45A05; 35B25; 35C20Domain (mathematical analysis)Settore MAT/05 - Analisi MatematicaSituated[MATH.MATH-AP]Mathematics [math]/Analysis of PDEs [math.AP]Dirichlet problem; Laplace operator; multiscale asymptotic expansion; real analytic continuation in Banach space; singularly perturbed perforated domainSmall hole[MATH]Mathematics [math]0101 mathematicsRepresentation (mathematics)MathematicsDirichlet problemDirichlet problemApplied Mathematics010102 general mathematicsMathematical analysisA domain010101 applied mathematicssingularly perturbed perforated domainLaplace operatorLaplace operatorAnalysisreal analytic continuation in Banach space
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RNA-mediated therapies in myotonic dystrophy

2018

Myotonic dystrophy 1 (DM1) is a multisystemic neuromuscular disease caused by a dominantly inherited 'CTG' repeat expansion in the gene encoding DM Protein Kinase (DMPK). The repeats are transcribed into mRNA, which forms hairpins and binds with high affinity to the Muscleblind-like (MBNL) family of proteins, sequestering them from their normal function. The loss of function of MBNL proteins causes numerous downstream effects, primarily the appearance of nuclear foci, mis-splicing, and ultimately myotonia and other clinical symptoms. Antisense and other RNA-mediated technologies have been applied to target toxic-repeat mRNA transcripts to restore MBNL protein function in DM1 models, such as…

musculoskeletal diseases0301 basic medicinePharmacologycongenital hereditary and neonatal diseases and abnormalitiesMessenger RNAMyotonin-protein kinaseRNABiologymedicine.diseaseMyotoniaMyotonic dystrophyMyotonin-Protein KinaseCell biology03 medical and health sciences030104 developmental biologyDrug DiscoverymedicineAnimalsHumansMyotonic DystrophyRNARNA MessengerTrinucleotide repeat expansionGeneLoss functionDrug Discovery Today
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Derepressing muscleblind expression by miRNA sponges ameliorates myotonic dystrophy-like phenotypes in Drosophila

2016

AbstractMyotonic Dystrophy type 1 (DM1) originates from alleles of the DMPK gene with hundreds of extra CTG repeats in the 3′ untranslated region (3′ UTR). CUG repeat RNAs accumulate in foci that sequester Muscleblind-like (MBNL) proteins away from their functional target transcripts. Endogenous upregulation of MBNL proteins is, thus, a potential therapeutic approach to DM1. Here we identify two miRNAs, dme-miR-277 and dme-miR-304, that differentially regulate muscleblind RNA isoforms in miRNA sensor constructs. We also show that their sequestration by sponge constructs derepresses endogenous muscleblind not only in a wild type background but also in a DM1 Drosophila model expressing non-co…

musculoskeletal diseases0301 basic medicineUntranslated regioncongenital hereditary and neonatal diseases and abnormalitiesMotor ActivityBiologyMyotonic dystrophyArticle03 medical and health sciences0302 clinical medicineRNA IsoformsmicroRNAmedicineAnimalsDrosophila ProteinsMyotonic DystrophyRegulation of gene expressionGeneticsMultidisciplinaryWild typeNuclear Proteinsmedicine.diseaseMicroRNAsDrosophila melanogasterPhenotype030104 developmental biologyGene Expression RegulationFlight AnimalTrinucleotide Repeat ExpansionTrinucleotide repeat expansion030217 neurology & neurosurgeryDrosophila ProteinScientific Reports
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Expanded CCUG repeat RNA expression in Drosophila heart and muscle trigger Myotonic Dystrophy type 1-like phenotypes and activate autophagocytosis ge…

2016

AbstractMyotonic dystrophies (DM1–2) are neuromuscular genetic disorders caused by the pathological expansion of untranslated microsatellites. DM1 and DM2, are caused by expanded CTG repeats in the 3′UTR of the DMPK gene and CCTG repeats in the first intron of the CNBP gene, respectively. Mutant RNAs containing expanded repeats are retained in the cell nucleus, where they sequester nuclear factors and cause alterations in RNA metabolism. However, for unknown reasons, DM1 is more severe than DM2. To study the differences and similarities in the pathogenesis of DM1 and DM2, we generated model flies by expressing pure expanded CUG ([250]×) or CCUG ([1100]×) repeats, respectively, and compared …

musculoskeletal diseases0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesRNA SplicingScienceGene ExpressionBiologyMyotonic dystrophyMyotonin-Protein KinaseArticle03 medical and health sciencesGene expressionAutophagymedicineAnimalsMyotonic DystrophyMuscle SkeletalGeneDNA Repeat ExpansionMultidisciplinaryMyocardiumQRIntronRNAArrhythmias CardiacDNA Repeat Expansionmedicine.diseaseMolecular biologyDisease Models AnimalCell nucleus030104 developmental biologymedicine.anatomical_structureRNA splicingMedicineDrosophilaLocomotionScientific Reports
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miR-7 Restores Phenotypes in Myotonic Dystrophy Muscle Cells by Repressing Hyperactivated Autophagy

2019

International audience; Unstable CTG expansions in the 3' UTR of the DMPK gene are responsible for myotonic dystrophy type 1 (DM1) condition. Muscle dysfunction is one of the main contributors to DM1 mortality and morbidity. Pathways by which mutant DMPK trigger muscle defects, however, are not fully understood. We previously reported that miR-7 was downregulated in a DM1 Drosophila model and in biopsies from patients. Here, using DM1 and normal muscle cells, we investigated whether miR-7 contributes to the muscle phenotype by studying the consequences of replenishing or blocking miR-7, respectively. Restoration of miR-7 with agomiR-7 was sufficient to rescue DM1 myoblast fusion defects and…

musculoskeletal diseases0301 basic medicineoligonucleotidemuscle atrophyautophagyBiologyMyotonic dystrophyArticleMuscleblind03 medical and health scienceschemistry.chemical_compoundMyoblast fusion0302 clinical medicineDrug DiscoverymicroRNAmedicineMBNL1MyocyteMyotonic DystrophymiRNAtherapy[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyAutophagyUPS systemmiR-7medicine.diseasePhenotypeMuscle atrophyCell biology030104 developmental biologychemistry030220 oncology & carcinogenesisMolecular MedicineCTG expansionsmedicine.symptom[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Sense and Antisense DMPK RNA Foci Accumulate in DM1 Tissues during Development.

2015

International audience; Myotonic dystrophy type 1 (DM1) is caused by an unstable expanded CTG repeat located within the DMPK gene 3'UTR. The nature, severity and age at onset of DM1 symptoms are very variable in patients. Different forms of the disease are described, among which the congenital form (CDM) is the most severe. Molecular mechanisms of DM1 are well characterized for the adult form and involve accumulation of mutant DMPK RNA forming foci in the nucleus. These RNA foci sequester proteins from the MBNL family and deregulate CELF proteins. These proteins are involved in many cellular mechanisms such as alternative splicing, transcriptional, translational and post-translational regul…

musculoskeletal diseasesCCAAT-Enhancer-Binding Protein-deltacongenital hereditary and neonatal diseases and abnormalities[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiologylcsh:MedicineMice Transgenic[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human genetics[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMyotonin-Protein KinaseMice[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]AnimalsHumansMyotonic DystrophyRNA AntisenseRNA Messengerlcsh:ScienceMuscle SkeletalCell NucleusMyocardiumlcsh:R[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyBrainGene Expression Regulation DevelopmentalRNA-Binding Proteins[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyEmbryo MammalianAlternative SplicingDisease Models Animal[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAnimals Newborn[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]lcsh:QTrinucleotide Repeat ExpansionSignal TransductionResearch ArticlePloS one
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Muscleblind, BSF and TBPH are mislocalized in the muscle sarcomere of a Drosophila myotonic dystrophy model

2012

SummaryMyotonic dystrophy type 1 (DM1) is a genetic disease caused by the pathological expansion of a CTG trinucleotide repeat in the 3' UTR of the DMPK gene. In the DMPK transcripts, the CUG expansions sequester RNA-binding proteins into nuclear foci, including transcription factors and alternative splicing regulators such as MBNL1. MBNL1 sequestration has been associated with key features of DM1. However, the basis behind a number of molecular and histological alterations in DM1 remain unclear. To help identify new pathogenic components of the disease, we carried out a genetic screen using a Drosophila model of DM1 that expresses 480 interrupted CTG repeats, i(CTG)480, and a collection of…

musculoskeletal diseasesSarcomerescongenital hereditary and neonatal diseases and abnormalitiesNeuroscience (miscellaneous)lcsh:MedicineMedicine (miscellaneous)RNA-binding proteinGenes InsectBiologyMyotonic dystrophyGeneral Biochemistry Genetics and Molecular BiologyAnimals Genetically Modifiedchemistry.chemical_compoundImmunology and Microbiology (miscellaneous)RNA interferencelcsh:PathologymedicineMBNL1AnimalsDrosophila ProteinsHumansMyotonic DystrophyGeneticsMuscleslcsh:RAlternative splicingNuclear ProteinsRNA-Binding ProteinsEpistasis Geneticmedicine.diseaseDisease Models AnimalchemistryGene Knockdown TechniquesDrosophilaFemaleRNA InterferenceTrinucleotide repeat expansionTrinucleotide Repeat ExpansionDrosophila Proteinlcsh:RB1-214Genetic screenResearch ArticleDisease Models & Mechanisms
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Modeling of Myotonic Dystrophy Cardiac Phenotypes in

2018

After respiratory distress, cardiac dysfunction is the second most common cause of fatality associated with the myotonic dystrophy (DM) disease. Despite the prevalance of heart failure in DM, physiopathological studies on heart symptoms have been relatively scarce because few murine models faithfully reproduce the cardiac disease. Consequently, only a small number of candidate compounds have been evaluated in this specific phenotype. To help cover this gap Drosophila combines the amenability of its invertebrate genetics with the possibility of quickly acquiring physiological parameters suitable for meaningful comparisons with vertebrate animal models and humans. Here we review available des…

myotonic dystrophyNeurologycardiac dysfunctionCTG expansionCCTG expansionMini ReviewDrosophila disease modelMuscleblinddrugsFrontiers in neurology
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Impacto de las técnicas de reconstrucción multicapa vascularizadas en la cirugía endoscópica endonasal de base de cráneo

2015

Los abordajes endonasales endoscópicos expandidos (AEEE) son un conjunto de técnicas quirúrgicas, completamente endoscópicas, mediante las cuales se abordan lesiones de la base craneal a través del corredor anatómico que supone la cavidad nasal y senos paranasales. Las técnicas reconstructivas inicialmente utilizadas en el cierre de defectos generados tras AEEE, estuvieron basadas en la experiencia previa acumulada con las reparaciones endoscópicas de fístulas de LCR. Múltiples estudios han validado que las pequeñas fístulas de LCR pueden ser reconstruidas con una amplia variedad de injertos libres como hemos visto en apartados anteriores, alcanzado del cierre con éxito en el 95% de los pac…

neurocirugíarecostrucciónabordaje endonasal expandidoUNESCO::CIENCIAS MÉDICAS:CIENCIAS MÉDICAS [UNESCO]base de craneo
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