Search results for "EPS"

showing 10 items of 1777 documents

Diagnostic Targeted Resequencing in 349 Patients with Drug-Resistant Pediatric Epilepsies Identifies Causative Mutations in 30 Different Genes

2017

Targeted resequencing gene panels are used in the diagnostic setting to identify gene defects in epilepsy. We performed targeted resequencing using a 30-genes panel and a 95-genes panel in 349 patients with drug-resistant epilepsies beginning in the first years of life. We identified 71 pathogenic variants, 42 of which novel, in 30 genes, corresponding to 20.3% of the probands. In 66% of mutation positive patients seizures onset occurred before age 6 months. The 95-genes panel allowed a genetic diagnosis in 22 (6.3%) patients that would have otherwise been missed using the 30-gene panel. About 50% of mutations were identified in genes coding for sodium and potassium channel components. SCN2…

0301 basic medicineProbandMaleCDKL5Drug Resistancemedicine.disease_causeBioinformaticsEpilepsyAnticonvulsantSTXBP1Age of OnsetChildGenetics (clinical)AlleleMutationepilepsy; next-generation sequencing; gene panel; mutationPhenotypeMagnetic Resonance ImagingSettore MED/39 - Neuropsichiatria Infantile3. Good healthPhenotypeChild PreschoolAnticonvulsantsFemaleSequence AnalysisHumanAdolescentGenotypeGenetic Association StudieBiologyMECP203 medical and health sciencesGeneticgene panelGeneticsmedicineHumansGenetic Predisposition to DiseasePreschoolGeneAllelesGenetic Association StudiesGene Expression ProfilingInfant NewbornComputational BiologyInfantMolecular Sequence AnnotationDNASequence Analysis DNANewbornmedicine.disease030104 developmental biologyepilepsynext-generation sequencingmutation
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HCN1 mutation spectrum: from neonatal epileptic encephalopathy to benign generalized epilepsy and beyond

2018

International audience; Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels control neuronal excitability and their dysfunction has been linked to epileptogenesis but few individuals with neurological disorders related to variants altering HCN channels have been reported so far. In 2014, we described five individuals with epileptic encephalopathy due to de novo HCN1 variants. To delineate HCN1-related disorders and investigate genotype-phenotype correlations further, we assembled a cohort of 33 unpublished patients with novel pathogenic or likely pathogenic variants: 19 probands carrying 14 different de novo mutations and four families with dominantly inherited variants segre…

0301 basic medicineProbandMaleModels MolecularPotassium Channels[SDV]Life Sciences [q-bio]Medizinmedicine.disease_causeEpileptogenesisMembrane PotentialsEpilepsy0302 clinical medicineHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsMissense mutationChildGeneticsMutationMiddle AgedPhenotype3. Good healthTransmembrane domainclinical spectrum; epilepsy; HCN1; intellectual disability; ion channelintellectual disabilityChild PreschoolEpilepsy GeneralizedFemaleSpasms InfantileAdultAdolescentCHO CellsBiology03 medical and health sciencesYoung AdultCricetulusHCN1medicineAnimalsHumansGeneralized epilepsyGenetic Association StudiesAgedInfantmedicine.diseaseElectric Stimulationclinical spectrum030104 developmental biologyMutationion channelMutagenesis Site-DirectedepilepsyNeurology (clinical)030217 neurology & neurosurgery
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7q31.32 partial duplication: First report of a child with dysmorphism, autistic spectrum disorder, moderate intellectual disability and, epilepsy. Li…

2019

Abstract Introduction Duplication of long arm of chromosome 7(q) is uncommon. It may occur as “pure”, isolated anomaly or in association with other mutations involving the same or other chromosomes. “Pure” chromosome 7q duplication has recently been classified by segment involved: the interstitial, proximal, or distal segment of the arm. Attempts to correlate genotype with phenotype in each group has yielded questionable results even though intellective disability and minor dysmorphic features of variable types are typically seen. Material and Methods In a young boy showing minor facial dysmorphism, language delay, autistic spectrum disorder, epileptic seizures, behavioral disturbances and …

0301 basic medicineProbandPediatricsmedicine.medical_specialtyAutism Spectrum DisorderLanguage delayDevelopmental DisabilitiesIrritabilityChromosomes03 medical and health sciencesEpilepsy0302 clinical medicineIntellectual DisabilityGene duplicationIntellectual disabilityHumansMedicineGenetic Association StudiesChromosome 7 (human)Epilepsybusiness.industrymedicine.disease7q31.32 duplicationDysmorphism030104 developmental biologyAutistic spectrum disorderNeurologyAutism spectrum disorderPair 7Neurology (clinical)medicine.symptombusinessChromosomes Human Pair 7030217 neurology & neurosurgeryHumanEpilepsy Research
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Transcriptomic study of the toxic mechanism triggered by beauvericin in Jurkat cells

2018

Beauvericin (BEA), an ionophoric cyclic hexadepsipeptide mycotoxin, is able to increase oxidative stress by altering membrane ion permeability and uncoupling oxidative phosphorylation. A toxicogenomic study was performed to investigate gene expression changes triggered by BEA exposure (1.5, 3 and 5 mu M; 24 h) in Jurkat cells through RNA-sequencing and differential gene expression analysis. Perturbed gene expression was observed in a concentration dependent manner, with 43 differentially expressed genes (DEGs) overlapped in the three studied concentrations. Gene ontology (GO) analysis showed several biological processes related to electron transport chain, oxidative phosphorylation, and cel…

0301 basic medicineProgrammed cell deathCYTOCHROME-C RELEASEBCL-2 FAMILYCell Membrane PermeabilityRespiratory chainCell Culture TechniquesCASPASE-3 ACTIVATIONApoptosisOxidative phosphorylationCHO-K1 CELLSToxicologyJurkat cellsOxidative PhosphorylationElectron Transport03 medical and health sciencesJurkat CellsFUSARIUM MYCOTOXINSImmunotoxicologyDepsipeptidesHumansREAL-TIME PCROXIDATIVE STRESSTranscriptomicsCaspaseINDUCED APOPTOSISLEUKEMIA-CELLS030102 biochemistry & molecular biologybiologyDose-Response Relationship DrugChemistryJurkatGene Expression ProfilingBcl-2 familyDEATHGeneral MedicineBeauvericinToxicogenomicsCell biologyGene expression profiling030104 developmental biologyMitochondrial respiratory chainGene Ontologybiology.proteinRNA-seqTranscriptomeToxicology Letters
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Mechanisms of beauvericin toxicity and antioxidant cellular defense

2015

Beauvericin (BEA) is a secondary metabolite produced by many species of fungus Fusarium. This study determines the injury (cell viability, cell proliferation, mitochondrial membrane potential, cell death and DNA damage) and the intracellular defense mechanisms (catalase and superoxide dismutase) in Chinese Hamster ovary (CHO-K1) cells after BEA exposure. The results obtained in this study demonstrated that BEA induces cytotoxicity in a dose- and time-dependent manner in CHO-K1 cells. Moreover, disruption in mitochondrial enzymatic activity and cell proliferation has been observed after BEA exposure, which can lead or be consequence of cell death. BEA inhibits cell proliferation by arresting…

0301 basic medicineProgrammed cell deathCell SurvivalDNA damageApoptosisCHO CellsToxicologyAntioxidantsSuperoxide dismutase03 medical and health sciencesCricetulus0404 agricultural biotechnologyDepsipeptidesAnimalsViability assayCell ProliferationMembrane Potential MitochondrialbiologySuperoxide DismutaseCell growthChinese hamster ovary cell04 agricultural and veterinary sciencesGeneral MedicineCatalase040401 food scienceCell biology030104 developmental biologyBiochemistryApoptosisbiology.proteinIntracellularDNA DamageToxicology Letters
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Neurotoxicity of zearalenone’s metabolites and beauvericin mycotoxins via apoptosis and cell cycle disruption

2021

Cell cycle progression and programmed cell death are imposed by pathological stimuli of extrinsic or intrinsic including the exposure to neurotoxins, oxidative stress and DNA damage. All can cause abrupt or delayed cell death, inactivate normal cell survival or cell death networks. Nevertheless, the mechanisms of the neuronal cell death are unresolved. One of the cell deaths triggers which have been wildly studied, correspond to mycotoxins produced by Fusarium species, which have been demonstrated cytotoxicity and neurotoxicity through impairing cell proliferation, gene expression and induction of oxidative stress. The aim of present study was to analyze the cell cycle progression and cell …

0301 basic medicineProgrammed cell deathCellPopulationApoptosisToxicology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorDepsipeptidesmedicineHumansEstrogens Non-SteroidaleducationCell Proliferationeducation.field_of_studyCell growthCell CycleNeurotoxicityMycotoxinsCell cyclemedicine.diseaseMolecular biologyBeauvericin030104 developmental biologymedicine.anatomical_structurechemistryApoptosisZearalenone030217 neurology & neurosurgeryToxicology
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Development of a New Antileishmanial Aziridine-2,3-Dicarboxylate-Based Inhibitor with High Selectivity for Parasite Cysteine Proteases

2015

ABSTRACT Leishmaniasis is one of the major neglected tropical diseases of the world. Druggable targets are the parasite cysteine proteases (CPs) of clan CA, family C1 (CAC1). In previous studies, we identified two peptidomimetic compounds, the aziridine-2,3-dicarboxylate compounds 13b and 13e, in a series of inhibitors of the cathepsin L (CL) subfamily of the papain clan CAC1. Both displayed antileishmanial activity in vitro while not showing cytotoxicity against host cells. In further investigations, the mode of action was characterized in Leishmania major . It was demonstrated that aziridines 13b and 13e mainly inhibited the parasitic cathepsin B (CB)-like CPC enzyme and, additionally, ma…

0301 basic medicineProteasesPeptidomimeticAziridines030106 microbiologyAntiprotozoal AgentsCysteine Proteinase InhibitorsCathepsin BLeishmania mexicanaCathepsin BCathepsin L03 medical and health sciencesTh2 CellsPapainPharmacology (medical)Leishmania majorAmastigoteLeishmaniasisLeishmania majorPharmacologybiologyChemistry; Biosynthesisbiology.organism_classificationLeishmania030104 developmental biologyInfectious DiseasesBiochemistrybiology.proteinAntimicrobial Agents and Chemotherapy
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New aziridine-based inhibitors of cathepsin L-like cysteine proteases with selectivity for the Leishmania cysteine protease LmCPB2.8

2018

Abstract In the present work a series of aziridine-2,3-dicarboxylate inhibitors of papain-like cysteine proteases was designed, synthesized and tested. The compounds displayed selectivity for the parasitic protozoon Leishmania mexicana cathepsin L-like cysteine protease LmCPB2.8. The computational methods of homology modelling and molecular docking predicted some significant differences in the S2 pocket of LmCPB2.8 and cruzain, a related enzyme from Trypanosoma cruzi. Due to the presence of Tyr209 in LmCPB2.8 rather than Glu208 in cruzain sterically demanding, lipophilic ester groups (inhibitor 7d, 9d, 12d and 14d) are predicted to occupy the S2 pocket of the Leishmania protease, but do not…

0301 basic medicineProteasesStereochemistryCathepsin Lmedicine.medical_treatmentAziridinesLeishmania mexicana030106 microbiologyLeishmaniasis CutaneousCysteine Proteinase Inhibitors01 natural sciencesLeishmania mexicanaCathepsin L03 medical and health sciencesparasitic diseasesDrug DiscoverymedicineHumansLeishmaniasisLeishmaniaPharmacologyProteaseAntiparasitic Agentsbiology010405 organic chemistryChemistryOrganic ChemistryActive siteGeneral Medicinebiology.organism_classificationCysteine protease0104 chemical sciencesMolecular Docking SimulationDocking (molecular)biology.proteinCysteineEuropean Journal of Medicinal Chemistry
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MycoKey Round Table Discussions of Future Directions in Research on Chemical Detection Methods, Genetics and Biodiversity of Mycotoxins

2018

MycoKey, an EU-funded Horizon 2020 project, includes a series of “Roundtable Discussions” to gather information on trending research areas in the field of mycotoxicology. This paper includes summaries of the Roundtable Discussions on Chemical Detection and Monitoring of mycotoxins and on the role of genetics and biodiversity in mycotoxin production. Discussions were managed by using the nominal group discussion technique, which generates numerous ideas and provides a ranking for those identified as the most important. Four questions were posed for each research area, as well as two questions that were common to both discussions. Test kits, usually antibody based, were one major focus of the…

0301 basic medicineProteomicsSettore CHIM/01 - CHIMICA ANALITICAComputer scienceHealth Toxicology and MutagenesisBiodiversitylcsh:Medicinebiological controlmicrobiomeToxicology//purl.org/becyt/ford/1 [https]transcriptomicscommunication with non-scientistsA better understanding of metabolomics from the cellular to the ecosystem level is needed to inform and control mycotoxin production control and remediation. Antibody-based diagnostics have become an acceptable standard in many practical applications but sophisticated multi-mycotoxin detection protocols are the future for many official regulatory controls especially as the number of toxins that are regulated increases and need more standardization and cross-laboratory validation.antibodies2. Zero hungerGeneticsbiologyNominal groupBiodiversitymetabolomicsGeneral partnershipBiological controlAntibodiesBiological controlCommunication with non-scientists Metabolomics Microbiome Multi-mycotoxin detection protocols Nominal group discussion technique ProteomicsTranscriptomicsmulti-mycotoxin detection protocolsSettore AGR/12 - PATOLOGIA VEGETALECommunication with non-scientistsEnvironmental MonitoringNominal group discussion techniqueOpinionAntibodies03 medical and health sciencesMycotoxicologyBiointeractions and Plant HealthproteomicsFood supplyAnimalsHumansMetabolomicsnominal group discussion technique//purl.org/becyt/ford/1.6 [https]Transcriptomicsbusiness.industryResearchlcsh:RUsabilityMycotoxinsbiology.organism_classification030104 developmental biologyMulti-mycotoxin detection protocolsRound tableRankingMicrobiomeEPSbusinesscommunication with non-scientistToxins
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Lethal systemic and brain infection caused by Prototheca zopfii algae in a patient with acute myeloid leukemia

2021

Systemic protothecosis is an exceptionally rare cause of sepsis with few available therapeutic options. Here, we report on a female patient with newly diagnosed acute myeloid leukemia who died after start of chemotherapy due to a severe septic shock caused by a disseminated systemic infection with Prototheca zopfii including encephalitis.

0301 basic medicineProtothecosisMedicine (General)QH301-705.5medicine.medical_treatmentProtothecosis030106 microbiology030231 tropical medicinePrototheca zopfiiCase ReportMicrobiologySepsis03 medical and health sciences0302 clinical medicineR5-920medicineImmunodeficiencyBiology (General)ImmunodeficiencyChemotherapyLeukemiabusiness.industrySeptic shockMyeloid leukemiamedicine.diseaseLeukemiaInfectious DiseasesImmunologyEncephalitisbusinessEncephalitisMedical Mycology Case Reports
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