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showing 10 items of 11015 documents

Corrigendum: Intraventricular injections of mesenchymal stem cells activate endogenous functional remyelination in a chronic demyelinating murine mod…

2017

Current treatments for demyelinating diseases are generally only capable of ameliorating the symptoms, with little to no effect in decreasing myelin loss nor promoting functional recovery. Mesenchymal stem cells (MSCs) have been shown by many researchers to be a potential therapeutic tool in treating various neurodegenerative diseases, including demyelinating disorders. However, in the majority of the cases, the effect was only observed locally, in the area surrounding the graft. Thus, in order to achieve general remyelination in various brain structures simultaneously, bone marrow-derived MSCs were transplanted into the lateral ventricles (LVs) of the cuprizone murine model. In this manner…

0301 basic medicineCancer ResearchCellular differentiationImmunologyMesenchymal stem cellSubventricular zoneCell BiologyBiologyNeural stem cellCell biology03 medical and health sciencesCellular and Molecular NeuroscienceMyelin030104 developmental biology0302 clinical medicinemedicine.anatomical_structurenervous systemImmunologymedicineOriginal ArticleRemyelinationProgenitor cellDemyelinating Disorder030217 neurology & neurosurgeryCell deathdisease
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Constitutive psgl-1 correlates with cd30 and tcr pathways and represents a potential target for immunotherapy in anaplastic large t-cell lymphoma

2021

Simple Summary P-selectin glycoprotein ligand-1 (PSGL-1), coded by the SELPLG gene, is the major ligand of selectins and plays a pivotal role in tethering, rolling and extravasation of immune cells. PSGL-1 involvement in core molecular programs, such as SYK, PLCγ2, PI3Kγ or MAPK pathways, suggests additional functions beyond the modulation of cell trafficking. Recently, several studies identified a novel mechanism responsible for PSGL-1-mediated immune suppression in the tumor microenvironment and proved a novel concept of PSGL-1 as a critical checkpoint molecule for tumor immunotherapy. The immunotherapeutic approach has gained an ever-growing interest in the treatment of several hematolog…

0301 basic medicineCancer ResearchPTCLCD30medicine.medical_treatmentSykLymphoproliferative disordersBiologyALCL; ALK; CD30; Immunotherapy; PSGL-1; PTCL; TCRArticle03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesmedicineT-cell lymphomaPSGL-1RC254-282integumentary systemT-cell receptorNeoplasms. Tumors. Oncology. Including cancer and carcinogensImmunotherapymedicine.diseaseALCLLymphomaGene expression profiling030104 developmental biologyOncologyALK030220 oncology & carcinogenesisCD30Cancer researchImmunotherapyTCR
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Persistent immune stimulation exacerbates genetically driven myeloproliferative disorders via stromal remodeling

2017

Abstract Systemic immune stimulation has been associated with increased risk of myeloid malignancies, but the pathogenic link is unknown. We demonstrate in animal models that experimental systemic immune activation alters the bone marrow stromal microenvironment, disarranging extracellular matrix (ECM) microarchitecture, with downregulation of secreted protein acidic and rich in cysteine (SPARC) and collagen-I and induction of complement activation. These changes were accompanied by a decrease in Treg frequency and by an increase in activated effector T cells. Under these conditions, hematopoietic precursors harboring nucleophosmin-1 (NPM1) mutation generated myeloid cells unfit for normal …

0301 basic medicineCancer ResearchStromal cellMyeloidMice TransgenicVascular RemodelingBiologyInbred C57BLTransgenicMice03 medical and health sciencesMyelogenousMyeloproliferative DisordersmedicineAnimalsHumansMyeloproliferative DisorderAnimals; Cell Proliferation; Humans; Mice; Mice Inbred C57BL; Mice Inbred CBA; Mice Transgenic; Myeloproliferative Disorders; Stromal Cells; Vascular Remodeling; Oncology; Cancer ResearchCell ProliferationMyeloproliferative DisordersAnimalStromal CellInbred CBANeutrophil extracellular trapsmedicine.diseaseMice Inbred C57BLHaematopoiesisLeukemia030104 developmental biologymedicine.anatomical_structureOncologyImmunologyMice Inbred CBABone marrowStromal CellsNucleophosminHuman
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RBFOX1, encoding a splicing regulator, is a candidate gene for aggressive behavior

2020

The RBFOX1 gene (or A2BP1) encodes a splicing factor important for neuronal development that has been related to autism spectrum disorder and other neurodevelopmental phenotypes. Evidence from complementary sources suggests that this gene contributes to aggressive behavior. Suggestive associations with RBFOX1 have been identified in genome-wide association studies (GWAS) of anger, conduct disorder, and aggressive behavior. Nominal association signals in RBFOX1 were also found in an epigenome-wide association study (EWAS) of aggressive behavior. Also, variants in this gene affect temporal lobe volume, a brain area that is altered in several aggression-related phenotypes. In animals, this gen…

0301 basic medicineCandidate geneNeuroimagingRBFOX1Genome-wide association studyBiologyEpigenesis GeneticA2BP103 medical and health sciencesAll institutes and research themes of the Radboud University Medical Center0302 clinical medicineGeneticsmedicineAnimalsHumansPharmacology (medical)TranscriptomicsRBFOX1Genetic Association StudiesBiological PsychiatryRegulator genePharmacologyGeneticsNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]AggressionGenetic Variationmedicine.diseasePhenotypeAnimal modelsAggressionPsychiatry and Mental health030104 developmental biologyNeurologyAutism spectrum disorderEpigeneticsRBFOX1 GeneRNA Splicing FactorsNeurology (clinical)medicine.symptom030217 neurology & neurosurgeryGenome-Wide Association Study
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SLC20A1 Is Involved in Urinary Tract and Urorectal Development

2020

Previous studies in developing Xenopus and zebrafish reported that the phosphate transporter slc20a1a is expressed in pronephric kidneys. The recent identification of SLC20A1 as a monoallelic candidate gene for cloacal exstrophy further suggests its involvement in the urinary tract and urorectal development. However, little is known of the functional role of SLC20A1 in urinary tract development. Here, we investigated this using morpholino oligonucleotide knockdown of the zebrafish ortholog slc20a1a. This caused kidney cysts and malformations of the cloaca. Moreover, in morphants we demonstrated dysfunctional voiding and hindgut opening defects mimicking imperforate anus in human cloacal exs…

0301 basic medicineCandidate genePathologyMorpholinoPediatricsEmbryonalentwicklungBlasenekstrophieBladder exstrophyZebrabärbling0302 clinical medicinebladder exstrophy-epispadias complex; CAKUT; cloacal malformation; functional genetics; kidney formation; SLC20A1; urinary tract development; zebrafish developmentbladder exstrophy-epispadias complexUrinary tract; Growth and developmentZebrafishlcsh:QH301-705.5ZebrafishNiereOriginal Researchcloacal malformationKidney; EmbryologyPediatrikzebrafish developmentKidney; Growth and developmentReconstructive and regenerative medicine Radboud Institute for Molecular Life Sciences [Radboudumc 10]030220 oncology & carcinogenesisembryonic structuresfunctional geneticsmedicine.symptomSLC20A1medicine.medical_specialtyEpispadiasanimal structuresUrinary systemBiologyKidney cystsCell and Developmental Biology03 medical and health sciencesAll institutes and research themes of the Radboud University Medical Centermedicineddc:610CAKUTNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Cloaca; Abnormalitieskidney formationCell Biologymedicine.diseaseCloacal exstrophybiology.organism_classificationurinary tract developmentReconstructive and regenerative medicine Radboud Institute for Health Sciences [Radboudumc 10]Bladder exstrophy030104 developmental biologyCloaca (embryology)lcsh:Biology (General)Developmental BiologyFrontiers in Cell and Developmental Biology
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Daunorubicin reduces MBNL1 titration by expanded CUG repeat RNA and rescues cardiac dysfunctions in a Drosophila model of myotonic dystrophy

2018

International audience; Myotonic dystrophy (DM) is a dominantly inherited neuromuscular disorder caused by expression of mutant DMPK transcripts containing expanded CUG repeats. Pathogenic RNA sequesters the muscleblind-like (MBNL) proteins, causing alterations of RNA metabolism. Cardiac dysfunction represents the second most common cause of death in DM1 patients. However, the contribution of MBNL titration in DM1 cardiac dysfunction is unclear. We overexpressed Muscleblind (Mbl), Drosophila MBNL orthologue, in cardiomyocytes of DM1 model flies and observed a rescue of heart dysfunctions, which are characteristic of these model flies and resemble cardiac defects observed in patients. We als…

0301 basic medicineCardiac function curvecongenital hereditary and neonatal diseases and abnormalitiesDaunorubicin[SDV]Life Sciences [q-bio]Neuroscience (miscellaneous)Medicine (miscellaneous)BiologyMyotonic dystrophyGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmunology and Microbiology (miscellaneous)medicineMBNL1Daunorubicin HydrochlorideRNAmedicine.diseaseTrinucleotide repeat disorder3. Good healthCell biology[SDV] Life Sciences [q-bio]030104 developmental biologychemistryTrinucleotide repeat expansion030217 neurology & neurosurgerymedicine.drug
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Toxic Tau Oligomers Modulated by Novel Curcumin Derivatives

2019

AbstractThe pathological aggregation and accumulation of tau, a microtubule-associated protein, is a common feature amongst more than 18 different neurodegenerative diseases that are collectively known as tauopathies. Recently, it has been demonstrated that the soluble and hydrophobic tau oligomers are highly toxic in vitro due to their capacity towards seeding tau misfolding, thereby propagating the tau pathology seen across different neurodegenerative diseases. Modulating the aggregation state of tau oligomers through the use of small molecules could be a useful therapeutic strategy to target their toxicity, regardless of other factors involved in their formation. In this study, we screen…

0301 basic medicineCell biologyCurcuminCell SurvivalNeurotoxinsChemical biologyBiophysicsDrug Evaluation Preclinicallcsh:Medicinetau ProteinsProtein aggregationOligomerBiochemistryArticleBiophysical Phenomena03 medical and health scienceschemistry.chemical_compoundMiceProtein Aggregates0302 clinical medicineCell Line Tumormental disordersAnimalsHumanslcsh:ScienceNeuronsMultidisciplinaryCell DeathDrug discoveryDrug discoverySettore BIO/16 - Anatomia Umanalcsh:RSettore CHIM/06 - Chimica OrganicaSmall moleculeChemical biologyIn vitro3. Good healthTau protein Curcumin030104 developmental biologychemistryCell cultureBiophysicsCurcuminAlzheimerlcsh:QProtein Multimerization030217 neurology & neurosurgeryNeuroscience
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Grey Matter Microstructural Integrity Alterations in Blepharospasm Are Partially Reversed by Botulinum Neurotoxin Therapy.

2016

OBJECTIVE Benign Essential Blepharospasm (BEB) and hemifacial spasm (HFS) are the most common hyperkinetic movement disorders of facial muscles. Although similar in clinical presentation different pathophysiological mechanisms are assumed. Botulinum Neurotoxin (BoNT) is a standard evidence-based treatment for both conditions. In this study we aimed to assess grey matter microstructural differences between these two groups of patients and compared them with healthy controls. In patients we furthermore tracked the longitudinal morphometric changes associated with BoNT therapy. We hypothesized microstructural differences between the groups at the time point of maximum symptoms representation a…

0301 basic medicineCentral Nervous SystemMaleMovement disordersBotulinum ToxinsBlepharospasmlcsh:MedicineToxicologyPathology and Laboratory MedicineNervous SystemDiagnostic Radiology0302 clinical medicineMaterials PhysicsMedicine and Health SciencesToxinsLongitudinal StudiesGray Matterlcsh:ScienceMicrostructureMultidisciplinaryMovement DisordersRadiology and ImagingPhysicsMotor CortexBrainNeurodegenerative DiseasesAnatomyMiddle AgedMagnetic Resonance ImagingPathophysiologyBotulinum neurotoxinFacial musclesDystoniamedicine.anatomical_structureTreatment OutcomeNeurologyPhysical SciencesFemalePrimary motor cortexmedicine.symptomAnatomyResearch ArticleAdultmedicine.medical_specialtyImaging TechniquesBlepharospasmToxic AgentsBacterial ToxinsMaterials ScienceBotulinum ToxinGrey matterResearch and Analysis Methods03 medical and health sciencesDiagnostic MedicineOphthalmologymedicineHumansHemifacial SpasmDemographyAgedbusiness.industrylcsh:RBiology and Life SciencesCorrectionmedicine.disease030104 developmental biologyCross-Sectional StudiesFacePeople and Placeslcsh:QbusinessHead030217 neurology & neurosurgeryHemifacial spasmPloS one
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OFIP/KIAA0753 forms a complex with OFD1 and FOR20 at pericentriolar satellites and centrosomes and is mutated in one individual with oral-facial-digi…

2016

Item does not contain fulltext Oral-facial-digital (OFD) syndromes are rare heterogeneous disorders characterized by the association of abnormalities of the face, the oral cavity and the extremities, some due to mutations in proteins of the transition zone of the primary cilia or the closely associated distal end of centrioles. These two structures are essential for the formation of functional cilia, and for signaling events during development. We report here causal compound heterozygous mutations of KIAA0753/OFIP in a patient with an OFD VI syndrome. We show that the KIAA0753/OFIP protein, whose sequence is conserved in ciliated species, associates with centrosome/centriole and pericentrio…

0301 basic medicineCentriolecell-cycle progressionGene Expressionmedicine.disease_causeCiliopathieshuman-disease genemolecular characterizationbbs proteinsGenetics (clinical)Conserved SequenceCentriolesGeneticsMutationCiliumCiliary transition zoneMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]General MedicineOrofaciodigital Syndromes3. Good healthcentriolar satellitesmultiple sequence alignmentbasal body dockingFemaleMicrotubule-Associated ProteinsProtein BindingHeterozygoteMolecular Sequence DataBiology03 medical and health sciencesIntraflagellar transportCiliogenesis[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineHumansAmino Acid SequenceCiliaMolecular BiologyCentrosomeintraflagellar transportBase SequenceInfant NewbornProteins030104 developmental biologyCentrosomeMutationciliary transition zoneSequence Alignment[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyciliogenesis
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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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