Search results for "BN"

showing 10 items of 1136 documents

Neuroactive Steroids Reverse Tonic Inhibitory Deficits in Fragile X Syndrome Mouse Model

2018

Fragile X syndrome (FXS) is the most common form of inherited intellectual disability. A reduction in neuronal inhibition mediated by γ-aminobutyric acid type A receptors (GABAARs) has been implicated in the pathophysiology of FXS. Neuroactive steroids (NASs) are known allosteric modulators of GABAAR channel function, but recent studies from our laboratory have revealed that NASs also exert persistent metabotropic effects on the efficacy of tonic inhibition by increasing the protein kinase C (PKC)-mediated phosphorylation of the α4 and β3 subunits which increase the membrane expression and boosts tonic inhibition. We have assessed the GABAergic signaling in the hippocampus of fragile X ment…

0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyNeuroactive steroidGABAA receptor (GABAAR)fragile XInhibitory postsynaptic potentialTonic (physiology)lcsh:RC321-571tonic inhibition03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineInternal medicinemedicineMolecular Biologylcsh:Neurosciences. Biological psychiatry. NeuropsychiatryProtein kinase COriginal ResearchChemistryphosphorylationDentate gyrusFMR1030104 developmental biologyEndocrinologyMetabotropic receptorGABAergicneurosteroidbenzodiazepine030217 neurology & neurosurgeryNeuroscienceFrontiers in Molecular Neuroscience
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Clinical Guide and Update on Porphyrias.

2019

Physicians should be aware of porphyrias, which could be responsible for unexplained gastrointestinal, neurologic, or skin disorders. Despite their relative rarity and complexity, most porphyrias can be easily defined and diagnosed. They are caused by well-characterized enzyme defects in the complex heme biosynthetic pathway and are divided into categories of acute vs non-acute or hepatic vs erythropoietic porphyrias. Acute hepatic porphyrias (acute intermittent porphyria, variegate porphyria, hereditary coproporphyria, and aminolevulinic acid dehydratase deficient porphyria) manifest in attacks and are characterized by overproduction of porphyrin precursors, producing often serious abdomin…

0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyPorphyrinsGastrointestinal DiseasesVariegate porphyriaPorphobilinogenCongenital erythropoietic porphyriaGastroenterologySkin Diseases03 medical and health sciencesPorphyrias0302 clinical medicineInternal medicinemedicineHumansPorphyria cutanea tardaskin and connective tissue diseasesAcute intermittent porphyriaHepatologybusiness.industryHepatoerythropoietic porphyriaGastroenterologynutritional and metabolic diseasesAminolevulinic Acidmedicine.disease030104 developmental biologyHereditary coproporphyriaPorphyriaPractice Guidelines as Topic030211 gastroenterology & hepatologyErythropoietic protoporphyriaNervous System DiseasesbusinessGastroenterology
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The quality of life in girls with Rett syndrome

2016

Nowadays, quality of life is receiving an increasing attention in all scientific areas. Rett syndrome (RTT) is a rare neurological development, affecting mainly females. The congenital disease affects the central nervous system, and is one of the most common causes of severe intellectual disability. The aim of our study is to evaluate the effect of RTT on the quality of life of people who are affected. Both parents of 18 subjects, all female, diagnosed with RTT, took part in the research. Quality of life was assessed using the Italian version of the Impact of Childhood Illness Scale. This scale consists of 30 questions that investigate the effect of illness on children, parents and families…

0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtylcsh:RC435-571lcsh:MedicineRett syndromeArticle03 medical and health sciencesRett syndrome0302 clinical medicineQuality of lifelcsh:PsychiatryIntellectual disabilitymedicineMedical historyPsychiatrylcsh:Rmedicine.diseaseSettore MED/39 - Neuropsichiatria InfantilePsychiatry and Mental health030104 developmental biologyquality of lifeintellectual disabilityScale (social sciences)Congenital diseasePsychology030217 neurology & neurosurgeryMental Illness
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Reflections on the unexpected laboratory finding of hemorheological alterations observed in some haematological disorders

2021

Hyperviscosity syndrome is a clinical condition characterized by the slowing of blood flow through the vessels and it may be associated with several diseases. The nosographic classification of primary hyperviscosity conditions (Wells classification 1970) divided the primary hyperviscosity syndromes in polycythaemic, sclerocytemic and sieric. Recent and personal laboratory observations have highlighted an unexpected behaviour of the erythrocyte deformability observed in some haematological disorders such as polycythemia vera, multiple myeloma and monoclonal gammopathy of undetermined significance. The interest of this observation depends on the fact that up to now, according to the Wells cla…

0301 basic medicinemedicine.medical_specialtyLaboratory findingHyperviscosityMonoclonal gammopathy of undetermined significance030204 cardiovascular system & hematologyBiochemistryHyperviscosity syndromes03 medical and health sciences0302 clinical medicinePolycythemia veraMultiple myelomaErythrocyte DeformabilityHyperviscosity syndromemedicineAnimalsHumansIntensive care medicinePolycythemia VeraMultiple myelomabusiness.industryModels CardiovascularCell Biologymedicine.diseaseBlood Viscosity030104 developmental biologyAbnormalityCardiology and Cardiovascular MedicinebusinessMonoclonal gammopathy of undetermined significanceHaematological disorders
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Clinical whole-exome sequencing for the diagnosis of rare disorders with congenital anomalies and/or intellectual disability: substantial interest of…

2017

International audience; PurposeCongenital anomalies and intellectual disability (CA/ID) are a major diagnostic challenge in medical genetics—50% of patients still have no molecular diagnosis after a long and stressful diagnostic “odyssey.” Solo clinical whole-exome sequencing (WES) was applied in our genetics center to improve diagnosis in patients with CA/ID.MethodsThis retrospective study examined 416 consecutive tests performed over 3 years to demonstrate the effectiveness of periodically reanalyzing WES data. The raw data from each nonpositive test was reanalyzed at 12 months with the most recent pipeline and in the light of new data in the literature. The results of the reanalysis for …

0301 basic medicinemedicine.medical_specialtyPediatricsCongenital anomaliesIntellectual disabilityTranslational researchClinical WES dataCongenital Abnormalities03 medical and health sciencesRare DiseasesIntellectual disabilityDatabases GeneticExome SequencingmedicineHumansExomeGenetic Testing[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsExomeGenetics (clinical)Exome sequencingGenetic testingRetrospective Studiesmedicine.diagnostic_testbusiness.industryHigh-Throughput Nucleotide SequencingRetrospective cohort studySequence Analysis DNAmedicine.diseaseAdditional research3. Good health030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsWhole-exome sequencingPhysical therapyRaw databusiness
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Increased Muscleblind levels by chloroquine treatment improve myotonic dystrophy type 1 phenotypes in in vitro and in vivo models

2019

Myotonic dystrophy type 1 (DM1) is a life-threatening and chronically debilitating neuromuscular disease caused by the expansion of a CTG trinucleotide repeat in the 3′ UTR of the DMPK gene. The mutant RNA forms insoluble structures capable of sequestering RNA binding proteins of the Muscleblind-like (MBNL) family, which ultimately leads to phenotypes. In this work, we demonstrate that treatment with the antiautophagic drug chloroquine was sufficient to up-regulate MBNL1 and 2 proteins in Drosophila and mouse (HSA LR ) models and patient-derived myoblasts. Extra Muscleblind was functional at the molecular level and improved splicing events regulated by MBNLs in all disease models. In vivo,…

0301 basic medicinemusculoskeletal diseasesMaleRNA SplicingRNA-binding proteinBiologyMyotonic dystrophychloroquinemuscleblindMyoblasts03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineIn vivomedicineAutophagyMBNL1AnimalsDrosophila ProteinsHumansMyotonic DystrophytherapyMultidisciplinarymyotonic dystrophyMusclesRNANuclear ProteinsRNA-Binding ProteinsChloroquinemedicine.diseaseMyotoniaCell biologyDNA-Binding ProteinsDisease Models Animal030104 developmental biologyPhenotypechemistryPNAS PlusRNA splicingDrosophilaFemaleTrinucleotide repeat expansion030217 neurology & neurosurgery
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miR-23b and miR-218 silencing increase Muscleblind-like expression and alleviate myotonic dystrophy phenotypes in mammalian models

2018

Functional depletion of the alternative splicing factors Muscleblind-like (MBNL 1 and 2) is at the basis of the neuromuscular disease myotonic dystrophy type 1 (DM1). We previously showed the efficacy of miRNA downregulation in Drosophila DM1 model. Here, we screen for miRNAs that regulate MBNL1 and MBNL2 in HeLa cells. We thus identify miR-23b and miR-218, and confirm that they downregulate MBNL proteins in this cell line. Antagonists of miR-23b and miR-218 miRNAs enhance MBNL protein levels and rescue pathogenic missplicing events in DM1 myoblasts. Systemic delivery of these “antagomiRs” similarly boost MBNL expression and improve DM1-like phenotypes, including splicing alterations, histo…

0301 basic medicinemusculoskeletal diseasesMalecongenital hereditary and neonatal diseases and abnormalitiesScienceMyoblasts SkeletalGeneral Physics and AstronomyMice TransgenicBiologyMyotonic dystrophyGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineRNA interferencemicroRNAmedicineMBNL1Gene silencingAnimalsHumansMyotonic DystrophyGene SilencingRNA Messengerlcsh:ScienceMuscle Skeletal3' Untranslated RegionsMultidisciplinaryThree prime untranslated regionAlternative splicingQRNA-Binding ProteinsGeneral Chemistrymedicine.diseaseMyotoniaCell biologyUp-RegulationAlternative SplicingDisease Models AnimalMicroRNAs030104 developmental biologyPhenotypechemistrylcsh:Q030217 neurology & neurosurgeryHeLa CellsNature Communications
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Apert Syndrome With FGFR2 758 C > G Mutation: A Chinese Case Report

2018

Background: Apert syndrome is considered as one of the most common craniosynostosis syndromes with a prevalence of 1 in 65,000 individuals, and has a close relationship with point mutations in FGFR2 gene.Case report: Here, we described a Apert syndrome case, who was referred to genetic consultation in our hospital with the symptom of craniosynostosis and syndactyly of the hands and feet. Craniosynostosis, midfacial retrusion, steep wide forehead, larger head circumference, marked depression of the nasal bridge, short and wide nose and proptosis could be found obviously, apart from these, ears were mildly low compared with normal children and there was no cleft lip and palate. Mutation was i…

0301 basic medicinemusculoskeletal diseasesPediatricsmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesNasal bridgelcsh:QH426-470Case ReportApert syndromeCraniosynostosis03 medical and health sciencesExonsymbols.namesake0302 clinical medicineGeneticsmedicineSyndactylyGenetics (clinical)NoseSanger sequencingbusiness.industryPoint mutationmedicine.diseaseexons sequencingcraniosynostosislcsh:Genetics030104 developmental biologymedicine.anatomical_structureFGFR2genetic mutationsymbolsMolecular Medicinebusiness030217 neurology & neurosurgeryApert syndromeFrontiers in Genetics
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Therapeutic Potential of AntagomiR-23b for Treating Myotonic Dystrophy

2020

Myotonic dystrophy type 1 (DM1) is a chronically debilitating, rare genetic disease that originates from an expansion of a noncoding CTG repeat in the dystrophia myotonica protein kinase (DMPK) gene. The expansion becomes pathogenic when DMPK transcripts contain 50 or more repetitions due to the sequestration of the muscleblind-like (MBNL) family of proteins. Depletion of MBNLs causes alterations in splicing patterns in transcripts that contribute to clinical symptoms such as myotonia and muscle weakness and wasting. We previously found that microRNA (miR)-23b directly regulates MBNL1 in DM1 myoblasts and mice and that antisense technology (“antagomiRs”) blocking this microRNA (miRNA) boost…

0301 basic medicinemusculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesMyotonic dystrophyArticleantagomiR03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDrug DiscoverymicroRNAMedicineMBNL1AntagomirProtein kinase AmiRNAmyotonic dystrophybusiness.industrylcsh:RM1-950Muscle weaknessmedicine.diseaseMyotoniaMbnl1030104 developmental biologylcsh:Therapeutics. Pharmacologychemistry030220 oncology & carcinogenesisRNA splicingCancer researchHSALR miceMolecular Medicinemedicine.symptomDM1antisense oligonucleotidesbusinessMolecular Therapy: Nucleic Acids
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The MID1 protein is a central player during development and in disease.

2015

Loss-of-function mutations in the MID1 gene cause a rare monogenic disorder, Opitz BBB/G syndrome (OS), which is characterized by malformations of the ventral midline. The MID1 gene encodes the MID1 protein, which assembles a large microtubule-associated protein complex. Intensive research over the past several years has shed light on the function of the MID1 protein as a ubiquitin ligase and regulator of mTOR signalling and translational activator. As a central player in the cell MID1 has been implicated in the pathogenesis of various other disorders in addition to OS including cancer and neurodegenerative diseases. Influencing the activity of the MID1 protein complex is a promising new st…

0301 basic medicinephysiopathology [Huntington Disease]CarcinogenesisUbiquitin-Protein LigasesRegulatorDiseaseBiologyBioinformaticsmedicine.disease_causephysiopathology [Alzheimer Disease]Congenital AbnormalitiesPathogenesis03 medical and health sciencesMiceAlzheimer Diseasephysiology [Nuclear Proteins]medicineAnimalsHumansgenetics [Microtubule Proteins]ddc:610GenePI3K/AKT/mTOR pathwayActivator (genetics)Nuclear Proteinsgenetics [Nuclear Proteins]genetics [Transcription Factors]physiology [Transcription Factors]Ubiquitin ligase030104 developmental biologyHuntington DiseaseMutationbiology.proteinMicrotubule Proteinsphysiology [Microtubule Proteins]CarcinogenesisMid1 protein humanTranscription FactorsFrontiers in bioscience (Landmark edition)
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