Search results for "DEP"

showing 10 items of 10555 documents

Bioelectrical coupling in multicellular domains regulated by gap junctions: A conceptual approach.

2018

We review the basic concepts involved in bioelectrically-coupled multicellular domains, focusing on the role of membrane potentials (Vmem). In the first model, single-cell Vmem is modulated by two generic polarizing and depolarizing ion channels, while intercellular coupling is implemented via voltage-gated gap junctions. Biochemical and bioelectrical signals are integrated via a feedback loop between Vmem and the transcription and translation of a protein forming an ion channel. The effective rate constants depend on the single-cell Vmem because these potentials modulate the local concentrations of signaling molecules and ions. This electrochemically-based idealization of the complex bioph…

0301 basic medicinePhysicsMembrane potentialFinite volume methodBiophysicsGap junctionGap JunctionsDepolarizationGeneral MedicineFeedback loopInterconnectivityModels BiologicalIon ChannelsIonElectrophysiological PhenomenaMembrane Potentials03 medical and health sciences030104 developmental biologyElectrochemistryAnimalsHumansPhysical and Theoretical ChemistryBiological systemIon channelSignal TransductionBioelectrochemistry (Amsterdam, Netherlands)
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Intercellular Connectivity and Multicellular Bioelectric Oscillations in Nonexcitable Cells: A Biophysical Model

2018

Bioelectricity is emerging as a crucial mechanism for signal transmission and processing from the single-cell level to multicellular domains. We explore theoretically the oscillatory dynamics that result from the coupling between the genetic and bioelectric descriptions of nonexcitable cells in multicellular ensembles, connecting the genetic prepatterns defined over the ensemble with the resulting spatio-temporal map of cell potentials. These prepatterns assume the existence of a small patch in the ensemble with locally low values of the genetic rate constants that produce a specific ion channel protein whose conductance promotes the cell-polarized state (inward-rectifying channel). In this…

0301 basic medicinePhysicsMembrane potentialGeneral Chemical EngineeringConductanceIon Channel ProteinContext (language use)DepolarizationGeneral ChemistryArticleQuantitative Biology::Cell BehaviorCoupling (electronics)lcsh:Chemistry03 medical and health sciencesMulticellular organism030104 developmental biology0302 clinical medicinelcsh:QD1-999Cell polarityBiophysics030217 neurology & neurosurgery
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Managing adult patients with infectious diseases in emergency departments: international ID-IRI study.

2021

We aimed to explore factors for optimizing antimicrobial treatment in emergency departments. A single-day point prevalence survey was conducted on January 18, 2020, in 53 referral/tertiary hospitals in 22 countries. 1957 (17%) of 11557 patients presenting to EDs had infections. The mean qSOFA score was 0.37 +/- 0.74. Sepsis (qSOFA >= 2) was recorded in 218 (11.1%) patients. The mean qSOFA score was significantly higher in low-middle (1.48 +/- 0.963) compared to upper-middle (0.17 +/- 0.482) and high-income (0.36 +/- 0.714) countries ( P < 0.001). Eight (3.7%) patients with sepsis were treated as outpatients. The most common diagnoses were upper-respiratory (n = 877, 43.3%), lower-respirator…

0301 basic medicinePoint prevalence surveymedicine.medical_specialtyUrologic NeoplasmsReferralinternational ID-IRI study- JOURNAL OF CHEMOTHERAPY 2021 [Erdem H. Hargreaves S. ANKARALI H. ÇAŞKURLU H. Ceviker S. A. Bahar-Kacmaz A. Meric-Koc M. ALTINDİŞ M. Yildiz-Kirazaldi Y. Kizilates F. et al. -Managing adult patients with infectious diseases in emergency departments]medicine.drug_classOrgan Dysfunction Scores030106 microbiologyAntibioticsPractice Patternsemergency ; antibiotic ; elderly ; infection ; sepsis ; treatmentGlobal HealthelderlyCommunicable Diseasestreatment.SepsisHospital03 medical and health sciences0302 clinical medicineantibioticSepsismedicineHumansPharmacology (medical)Practice Patterns Physicians'Developing CountriesRespiratory Tract InfectionsPharmacologyEmergency ServicePhysicians'Adult patientstreatmentbusiness.industryPatient AcuityAntimicrobialmedicine.diseasehumanitiesinfectionDrug UtilizationAnti-Bacterial AgentsInfectious DiseasesOncology030220 oncology & carcinogenesisEmergency medicineEmergencysepsibusinessEmergency Service HospitalJournal of chemotherapy (Florence, Italy)
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Chemical probes to potently and selectively inhibit endocannabinoid cellular reuptake

2017

The extracellular effects of the endocannabinoids anandamide and 2-arachidonoyl glycerol are terminated by enzymatic hydrolysis after crossing cellular membranes by facilitated diffusion. The lack of potent and selective inhibitors for endocannabinoid transport has prevented the molecular characterization of this process, thus hindering its biochemical investigation and pharmacological exploitation. Here, we report the design, chemical synthesis, and biological profiling of natural product-derived N-substituted 2,4-dodecadienamides as a selective endocannabinoid uptake inhibitor. The highly potent (IC50 = 10 nM) inhibitor N-(3,4-dimethoxyphenyl)ethyl amide (WOBE437) exerted pronounced canna…

0301 basic medicinePolyunsaturated Alkamidesmedicine.drug_classmedicine.medical_treatmentAnti-Inflammatory AgentsArachidonic AcidsPharmacologyDepolarization-induced suppression of inhibitionAnxiolyticGlyceridesReuptakeMice03 medical and health scienceschemistry.chemical_compoundCell Line TumorExtracellularmedicineAnimalsHumansReceptors Cannabinoid610 Medicine &amp; healthMice Inbred BALB CMultidisciplinaryHydrolysismusculoskeletal neural and ocular physiologyCell MembraneBrainBiological TransportU937 CellsAnandamideMembrane transportEndocannabinoid systemMice Inbred C57BL030104 developmental biologynervous systemPNAS PlusAnti-Anxiety AgentschemistryBiophysics570 Life sciences; biologylipids (amino acids peptides and proteins)Cannabinoidpsychological phenomena and processesEndocannabinoidsProceedings of the National Academy of Sciences
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Microbiome restoration diet improves digestion, cognition and physical and emotional wellbeing

2017

Manipulating gut bacteria in the microbiome, through the use of probiotics and prebiotics, has been found to have an influence on both physical and emotional wellbeing. This study uses a dietary manipulation 'The Gut Makeover' designed to elicit positive changes to the gut bacteria within the microbiome. 21 healthy participants undertook 'The Gut Makeover' for a four week period. Weight and various aspects of health were assessed pre and post intervention using the Functional Medicine Medical Symptoms Questionnaire (MSQ). Paired sample t-tests revealed a significant reduction in self-reported weight at the end of the intervention. Adverse medical symptoms related to digestion, cognition and…

0301 basic medicinePopulationEmotionslcsh:MedicineSocial SciencesDiseaseMicrobial GenomicsAnxietyMicrobiology03 medical and health sciencesIntervention (counseling)Mental Health and PsychiatryGeneticsMedicine and Health SciencesMedicinePsychologyMicrobiomelcsh:ScienceeducationNutritioneducation.field_of_studyFunctional medicineMultidisciplinaryBacteriabusiness.industryMood DisordersDepressionProbioticslcsh:RGut BacteriaOrganismsBiology and Life SciencesCognitionGenomicsMental healthDiet030104 developmental biologyMedical MicrobiologyAnxietylcsh:QMicrobiomemedicine.symptombusinessClinical psychologyResearch ArticlePLoS ONE
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A systematic variant screening in familial cases of congenital heart defects demonstrates the usefulness of molecular genetics in this field

2016

International audience; The etiology of congenital heart defect (CHD) combines environmental and genetic factors. So far, there were studies reporting on the screening of a single gene on unselected CHD or on familial cases selected for specific CHD types. Our goal was to systematically screen a proband of familial cases of CHD on a set of genetic tests to evaluate the prevalence of disease-causing variant identification. A systematic screening of GATA4, NKX2-5, ZIC3 and Multiplex ligation-dependent probe amplification (MLPA) P311 Kit was setup on the proband of 154 families with at least two cases of non-syndromic CHD. Additionally, ELN screening was performed on families with supravalvula…

0301 basic medicineProbandMaleCardiomyopathy22q11.2Disease030204 cardiovascular system & hematologyBioinformatics0302 clinical medicinede-novoEpidemiology3 large registriesGenetics (clinical)zic3 mutationsGeneticsHigh-Throughput Nucleotide Sequencing3. Good healthPedigreeHomeobox Protein Nkx-2.5malformationsFemaleepidemiologyHeart Defects Congenitalmedicine.medical_specialtyGenetic counselingArticle03 medical and health sciences[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyMolecular geneticsGeneticsmedicineHumansMultiplex ligation-dependent probe amplificationGenetic TestingHomeodomain Proteinsdiseasebusiness.industryvariabilityGenetic Variationmedicine.diseaseGATA4 Transcription Factor030104 developmental biologyMutationEtiologycardiovascular defectsbusinessMultiplex Polymerase Chain Reactioncardiomyopathy[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyTranscription Factors
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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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Aβ Induces Excitotoxicity Mediated by APC/C-Cdh1 Depletion That Can Be Prevented by Glutaminase Inhibition Promoting Neuronal Survival

2016

AbstractThe E3 ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C) is activated by the fizzy-related protein homolog/CDC20-like protein 1 (cdh1) in post-mitotic neurons. Growing evidence suggests that dysregulation of APC/C-Cdh1 is involved in neurodegenerative diseases. Here we show in neurons that oligomers of amyloid beta (Aβ), a peptide related to Alzheimer’s disease, cause proteasome-dependent degradation of cdh1. This leads to a subsequent increase in glutaminase (a degradation target of APC/C-Cdh1), which causes an elevation of glutamate levels and further intraneuronal Ca2+ dysregulation, resulting in neuronal apoptosis. Glutaminase inhibition prevents glutamate excitotoxi…

0301 basic medicineProteasome Endopeptidase ComplexCell SurvivalAmyloid betaBlotting WesternExcitotoxicityHippocampusmedicine.disease_causeHippocampusArticleAnaphase-Promoting Complex-CyclosomeCdh1 ProteinsAnimals Genetically ModifiedMice03 medical and health sciences0302 clinical medicineGlutaminasemedicineAnimalsRats WistarNeuronsAmyloid beta-PeptidesMultidisciplinarybiologyGlutaminaseCyclin-dependent kinase 5Glutamate receptorCyclin-Dependent Kinase 5Molecular biologyRatsUbiquitin ligase030104 developmental biologyApoptosisbiology.protein030217 neurology & neurosurgeryScientific Reports
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