Search results for " and neonatal diseases and abnormalities"

showing 10 items of 344 documents

Sustained activation of mTOR pathway in embryonic neural stem cells leads to development of tuberous sclerosis complex-associated lesions

2011

SummaryTuberous Sclerosis Complex (TSC) is a multisystem genetic disorder characterized by hamartomatous neurological lesions that exhibit abnormal cell proliferation and differentiation. Hyperactivation of mTOR pathway by mutations in either the Tsc1 or Tsc2 gene underlies TSC pathogenesis, but involvement of specific neural cell populations in the formation of TSC-associated neurological lesions remains unclear. We deleted Tsc1 in Emx1-expressing embryonic telencephalic neural stem cells (NSCs) and found that mutant mice faithfully recapitulated TSC neuropathological lesions, such as cortical lamination defects and subependymal nodules (SENs). These alterations were caused by enhanced gen…

Telencephaloncongenital hereditary and neonatal diseases and abnormalitiesCellular differentiationNeuroepithelial CellsEmbryonic DevelopmentBiologyTuberous Sclerosis Complex 1 Proteinmurine modelCerebral VentriclesMiceNeural Stem CellsCell MovementTuberous SclerosismedicineGeneticsAnimalsAnimals; Animals Newborn; Cell Differentiation; Cell Movement; Cell Proliferation; Cerebral Ventricles; Embryonic Development; Embryonic Stem Cells; Epilepsy; Gene Silencing; Gene Targeting; Megalencephaly; Mice; Mutation; Neural Stem Cells; Neuroepithelial Cells; Neurons; TOR Serine-Threonine Kinases; Telencephalon; Tuberous Sclerosis; Tuberous Sclerosis Complex 1 Protein; Tumor Suppressor Proteins; Signal TransductionGene SilencingNeural cellPI3K/AKT/mTOR pathwayEmbryonic Stem CellsCell ProliferationNeuronsEpilepsymTOR; Neural Stem Cells; Tuberous Sclerosis; murine modelTOR Serine-Threonine KinasesTumor Suppressor ProteinsCell DifferentiationCell BiologyNewbornEmbryonic stem cellNeural stem cellMegalencephalyCell biologynervous system diseasesNeuroepithelial cellmedicine.anatomical_structureAnimals NewbornImmunologyGene TargetingMutationmTORMolecular MedicineTSC1TSC2Signal Transduction
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Effect of halloysite nanotubes filler on polydopamine properties

2019

Abstract Hypothesis Polydopamine (PDA) is widely used as hydrophilic coating for several applications. However, most of the methods studied to improve or manipulate PDA properties are multistep and time-consuming, and there is a need for versatile strategies aimed at controlling and modifying the properties of PDA. Experiments PDA-halloysite nanocomposites were produced under different oxidation conditions in alkaline and acidic media and were characterized by UV–visible and attenuated total refraction- Fourier Transform Infrared spectroscopies, thermogravimetric analysis, porosimetry, scanning electron microscopy, X-ray diffraction and contact angle measurements against the reference PDA p…

Thermogravimetric analysiscongenital hereditary and neonatal diseases and abnormalitiesPolydopamineMaterials scienceScanning electron microscopeeducationHalloysite nanotube02 engineering and technologyengineering.material010402 general chemistry01 natural sciencesHalloysiteBiomaterialsContact angleColloid and Surface ChemistryAdsorptionhealth services administrationSettore CHIM/02 - Chimica FisicaNanocompositeNanocompositeEnvironmental remediationPorosimetrySettore CHIM/06 - Chimica Organica021001 nanoscience & nanotechnology0104 chemical sciencesSurfaces Coatings and FilmsElectronic Optical and Magnetic MaterialsMembraneChemical engineeringengineeringPolydopamine Halloysite nanotubes Nanocomposite Environmental remediation0210 nano-technology
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The Wilms' tumor suppressor gene (wt1) product regulates Dax-1 gene expression during gonadal differentiation.

1999

Gonadal differentiation is dependent upon a molecular cascade responsible for ovarian or testicular development from the bipotential gonadal ridge. Genetic analysis has implicated a number of gene products essential for this process, which include Sry, WT1, SF-1, and DAX-1. We have sought to better define the role of WT1 in this process by identifying downstream targets of WT1 during normal gonadal development. We have noticed that in the developing murine gonadal ridge, wt1 expression precedes expression of Dax-1, a nuclear receptor gene. We document here that the spatial distribution profiles of both proteins in the developing gonad overlap. We also demonstrate that WT1 can activate the D…

Transcriptional Activationcongenital hereditary and neonatal diseases and abnormalitiesGenes Wilms TumorReceptors Retinoic AcidTATA boxMolecular Sequence DataMutagenesis (molecular biology technique)Biologyurologic and male genital diseasesResponse ElementsTransactivationMiceGene expressionAnimalsHumansGonadsPromoter Regions GeneticWT1 ProteinsMolecular BiologyGeneCell Growth and DevelopmentCell Line TransformedGonadal ridgeBase Sequenceurogenital systemDAX-1 Orphan Nuclear ReceptorfungiGene Expression Regulation DevelopmentalCell Biologyfemale genital diseases and pregnancy complicationsCell biologyDNA-Binding ProteinsRepressor ProteinsTestis determining factorNuclear receptorCOS CellsCancer researchTranscription FactorsMolecular and cellular biology
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Physiological activation of the IgH 3' enhancer in B lineage cells is not blocked by Pax-5.

1996

The mouse 3' enhancer contains a high-affinity binding site for the paired box protein Pax-5. Here, we demonstrate by genomic footprinting that the rat 3' enhancer contains a low-affinity binding site for Pax-5, which is occupied in activated splenic B cells. Thus, binding of Pax-5 to the IgH 3' enhancer appears to be evolutionarily conserved in rodents. Analysis of Pax-5 expression in primary B cells demonstrates that Pax-5 remains expressed after 4 days of lipopolysaccharide (LPS) induction, but is down-regulated in 5-day stimulated cells. Similarly, the expression of Pax-5 is down-regulated in vivo in activated large splenocytes, in contrast to small resting cells. Multimerization of the…

Transcriptional Activationcongenital hereditary and neonatal diseases and abnormalitiesanimal structuresImmunologyCD40 LigandDNA FootprintingHeterologousDown-RegulationReceptors Antigen B-CellEnhancer RNAsLymphocyte ActivationMiceGene expressionImmunology and AllergyAnimalsBinding siteEnhancerTranscription factorCells CulturedReporter geneB-LymphocytesCD40Membrane GlycoproteinsbiologyGenes ImmunoglobulinPAX5 Transcription FactorNuclear ProteinsMolecular biologyRatsUp-Regulationbody regionsDNA-Binding ProteinsRepressor ProteinsEnhancer Elements GeneticGene Expression Regulationembryonic structuresbiology.proteinTrans-Activatorssense organsTranscription FactorsEuropean journal of immunology
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Design of novel small molecule base-pair recognizers of toxic CUG RNA transcripts characteristics of DM1.

2020

Graphical abstract

Untranslated regioncongenital hereditary and neonatal diseases and abnormalitiesBase pairMyotonic dystrophyBiophysicsComputational biologyBase recognitionBiologyBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineStructural BiologyRNA targetingGeneticsMBNL1030304 developmental biologyComputingMethodologies_COMPUTERGRAPHICS0303 health sciencesDrug discoveryAlternative splicingRNABiological activityNon-coding RNAComputer Science Applicationschemistry030220 oncology & carcinogenesisMolecular modellingTP248.13-248.65Small moleculeBiotechnologyResearch ArticleComputational and structural biotechnology journal
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Myotonic dystrophy associated expanded CUG repeat muscleblind positive ribonuclear foci are not toxic to Drosophila

2005

Myotonic dystrophy type 1 is an autosomal dominant disorder associated with the expansion of a CTG repeat in the 3 0 untranslated region (UTR) of the DMPK gene. Recent data suggest that pathogenesis is predominantly mediated by a gain of function of the mutant transcript. In patients, these expanded CUG repeat-containing transcripts are sequestered into ribonuclear foci that also contain the muscleblind-like proteins. To provide further insights into muscleblind function and the pathogenesis of myotonic dystrophy, we generated Drosophila incorporating CTG repeats in the 3 0 -UTR of a reporter gene. As in patients, expanded CUG repeats form discrete ribonuclear foci in Drosophila muscle cell…

Untranslated regioncongenital hereditary and neonatal diseases and abnormalitiesRNA StabilityProtein Serine-Threonine KinasesBiologyMyotonic dystrophyMyotonin-Protein KinaseGeneticsmedicineAnimalsHumansMyotonic Dystrophy3' Untranslated RegionsMolecular BiologyGeneGenetics (clinical)GeneticsRNAGeneral MedicineNuclear matrixbiology.organism_classificationmedicine.diseaseCell biologyRNA silencingDrosophila melanogasterRNA splicingDrosophila melanogasterTrinucleotide Repeat ExpansionHuman Molecular Genetics
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Pentamidine rescues contractility and rhythmicity in a Drosophila model of myotonic dystrophy heart dysfunction

2015

Up to 80% of individuals with myotonic dystrophy type 1 (DM1) will develop cardiac abnormalities at some point during the progression of their disease, the most common of which is heart blockage of varying degrees. Such blockage is characterized by conduction defects and supraventricular and ventricular tachycardia, and carries a high risk of sudden cardiac death. Despite its importance, very few animal model studies have focused on the heart dysfunction in DM1. Here, we describe the characterization of the heart phenotype in a Drosophila model expressing pure expanded CUG repeats under the control of the cardiomyocyte-specific driver GMH5-Gal4. Morphologically, expression of 250 CUG repeat…

[SDV]Life Sciences [q-bio]Myotonic dystrophyMedicine (miscellaneous)lcsh:MedicineVentricular tachycardiaImmunology and Microbiology (miscellaneous)DiastoleHeart RateDrosophila ProteinsMyocytes CardiacGeneticsbiologyRNuclear ProteinsHeartPhenotype3. Good healthCell biology[SDV] Life Sciences [q-bio]Drosophila melanogasterPhenotypeDrosophilaDrosophila melanogasterDrosophila ProteinResearch Articlelcsh:RB1-214congenital hereditary and neonatal diseases and abnormalitiesSystoleLongevityNeuroscience (miscellaneous)In situ hybridizationMyotonic dystrophyGeneral Biochemistry Genetics and Molecular BiologyMuscleblindContractilitymedicinelcsh:PathologyAnimalsPentamidineHeart dysfunctionfungilcsh:RArrhythmias Cardiacbiology.organism_classificationmedicine.diseaseMyocardial ContractionSurvival AnalysisDisease Models AnimalTrinucleotide repeat expansionTrinucleotide Repeat Expansion
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Segmentation et métrologie des sinus de Valsalva à partir de ciné-IRM

2012

Automatic segmentation of Valsalva sinuses from cine-MRI

body regionscongenital hereditary and neonatal diseases and abnormalities[ INFO.INFO-IM ] Computer Science [cs]/Medical Imaging[INFO.INFO-IM] Computer Science [cs]/Medical Imagingcardiovascular system[INFO.INFO-IM]Computer Science [cs]/Medical Imagingcardiovascular diseasescirculatory and respiratory physiology
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No Difference in Penetrance between Truncating and Missense/Aberrant Splicing Pathogenic Variants in MLH1 and MSH2: A Prospective Lynch Syndrome Data…

2021

Background. Lynch syndrome is the most common genetic predisposition for hereditary cancer. Carriers of pathogenic changes in mismatch repair (MMR) genes have an increased risk of developing colorectal (CRC), endometrial, ovarian, urinary tract, prostate, and other cancers, depending on which gene is malfunctioning. In Lynch syndrome, differences in cancer incidence (penetrance) according to the gene involved have led to the stratification of cancer surveillance. By contrast, any differences in penetrance determined by the type of pathogenic variant remain unknown. Objective. To determine cumulative incidences of cancer in carriers of truncating and missense or aberrant splicing pathogenic …

cancer incidence0302 clinical medicineMalalties hereditàriesMissense mutation8Q23.3CàncerCancerGenetics0303 health sciencesmedicine.diagnostic_testFactors de risc en les malaltiesMISMATCH REPAIR GENESRMLH1General MedicinePenetranceLynch syndrome3. Good healthsyöpägeenit030220 oncology & carcinogenesisMedicinesyöpätauditilmaantuvuusGenetic diseasescongenital hereditary and neonatal diseases and abnormalitiesmissense11Q23.1Risk factors in diseasesCANCER-RISKMLH1Articleaberrant splicing03 medical and health sciencesAGEmedicineGenetic predispositionddc:610<i>MSH2</i>Lynchin oireyhtymäpenetrance030304 developmental biologyGenetic testingMLH1; MSH2; penetrance; cancer incidence; truncating; missense; aberrant splicing; Lynch syndromeperinnölliset tauditbusiness.industryMUTATIONSHMSH2Cancernutritional and metabolic diseasesmedicine.diseasedigestive system diseasesMSH2Lynch syndromeMSH23121 General medicine internal medicine and other clinical medicine<i>MLH1</i>businesstruncating
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Impact of Fragile X Syndrome on Their Families

2020

espanolEl objetivo del presente estudio es describir las alteraciones conductuales y emocionales en el sindrome de X fragil (SXF) y analizar las reperecusiones de tener un miembro con SXF en diferentes aspectos del funcionamiento familiar. Participaron 79 padres con un miembro con SXF y 80 padres con un miembro con desarrollo tipico. Los resultados mostraron que entre el 17% y el 66% de los ninos y adolescentes con SXF mostraron trastornos conductuales y emocionales significativos y menos comportamientos prosociales. Ademas, despues de controlar las dificultades emocionales y de comportamiento, nuestros resultados mostraron que las familias afectadas por SXF experimentaron un impacto mas ne…

congenital hereditary and neonatal diseases and abnormalities030506 rehabilitationfamilySocial Psychologyfragile x syndromeFamily functioninglcsh:BF1-990trastorno de la conductaanálisis comparativo03 medical and health sciencesDevelopmental and Educational Psychologymedicine0501 psychology and cognitive sciencessituación familiar05 social sciencesSíndrome X Frágil (SXF)vida familiarmedicine.diseaseSindrome deFragile X syndromeClinical Practicelcsh:Psychologylcsh:Bimpactlcsh:Philosophy. Psychology. Religion0305 other medical sciencePsychologyHumanitiestrastorno emocional050104 developmental & child psychologyPsicología Educativa
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