Search results for "Nerve degeneration"

showing 10 items of 62 documents

The

2016

ABSTRACT Members of the Junctophilin (JPH) protein family have emerged as key actors in all excitable cells, with crucial implications for human pathophysiology. In mammals, this family consists of four members (JPH1-JPH4) that are differentially expressed throughout excitable cells. The analysis of knockout mice lacking JPH subtypes has demonstrated their essential contribution to physiological functions in skeletal and cardiac muscles and in neurons. Moreover, mutations in the human JPH2 gene are associated with hypertrophic and dilated cardiomyopathies; mutations in JPH3 are responsible for the neurodegenerative Huntington's disease-like-2 (HDL2), whereas JPH1 acts as a genetic modifier …

NotchGenotypeCardiomyopathyGenes InsectAnimals Genetically ModifiedAnimalsDrosophila ProteinsAllelesMammalsNeuronsHuntingtin ProteinReceptors NotchMusclesMyocardiumMembrane ProteinsReproducibility of ResultsDrosHuntington's diseaseDisease Models AnimalDrosophila melanogasterPhenotypeGene Knockdown TechniquesMutationNerve DegenerationPhotoreceptor Cells InvertebrateRNA InterferenceJunctophilinDrosophilaTrinucleotide Repeat ExpansionSignal TransductionResearch ArticleDisease modelsmechanisms
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Molecular partners of hNOT/ALG3, the human counterpart of the Drosophila NOT and yeast ALG3 gene, suggest its involvement in distinct cellular proces…

2018

This study provides first insights into the involvement of hNOT/ALG3, the human counterpart of the Drosophila Neighbour of TID and yeast ALG3 gene, in various putative molecular networks. HNOT/ALG3 encodes two translated transcripts encoding precursor proteins differing in their N-terminus and showing 33% identity with the yeast asparagine-linked glycosylation 3 (ALG3) protein. Experimental evidence for the functional homology of the proteins of fly and man in the N-glycosylation has still to be provided. In this study, using the yeast two-hybrid technique we identify 17 molecular partners of hNOT-1/ALG3-1. We disclose the building of hNOT/ALG3 homodimers and provide experimental evidence f…

0301 basic medicineGlycosylationSaccharomyces cerevisiae ProteinsRNA-binding proteinSaccharomyces cerevisiaeBiologyEndoplasmic ReticulumMannosyltransferases03 medical and health scienceschemistry.chemical_compoundCongenital Disorders of GlycosylationNeoplasmsNuclear Receptor Subfamily 4 Group A Member 2GeneticsAnimalsDrosophila ProteinsHumansMolecular BiologyTranscription factorOSBPGeneGenetics (clinical)Cellular compartmentEndoplasmic reticulumMembrane ProteinsRNA-Binding ProteinsGeneral MedicineLRP1Cell biology030104 developmental biologychemistryNerve DegenerationDrosophilaCarrier ProteinsHuman molecular genetics
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Depletion of polysialic acid from neural cell adhesion molecule (PSA-NCAM) increases CA3 dendritic arborization and increases vulnerability to excito…

2012

Chronic immobilization stress (CIS) shortens apical dendritic trees of CA3 pyramidal neurons in the hippocampus of the male rat, and dendritic length may be a determinant of vulnerability to stress. Expression of the polysialylated form of neural cell adhesion molecule (PSA-NCAM) in the hippocampal formation is increased by stress, while PSA removal by Endo-neuraminidase-N (endo-N) is known to cause the mossy fibers to defasciculate and synapse ectopically in their CA3 target area. We show here that enzymatic removal of PSA produced a remarkable expansion of dendritic arbors of CA3 pyramidal neurons, with a lesser effect in CA1. This expansion eclipsed the CIS-induced shortening of CA3 dend…

MaleSilver StainingKainic acidExcitotoxicityHippocampusBiologyHippocampal formationmedicine.disease_causeReceptors N-Methyl-D-AspartateArticleBody Mass IndexRats Sprague-DawleySynapsechemistry.chemical_compoundDevelopmental NeuroscienceExcitatory Amino Acid AgonistsmedicineAnimalsOrganic ChemicalsReceptorNeural Cell Adhesion MoleculesAnalysis of VarianceKainic AcidPolysialic acidPyramidal CellsMetalloendopeptidasesDendritesFluoresceinsCA3 Region HippocampalRatsCell biologyDisease Models AnimalGene Expression Regulationnervous systemNeurologychemistryNerve DegenerationSialic AcidsNeural cell adhesion moleculeNeuroscienceStress PsychologicalExperimental Neurology
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Xenon improves long-term cognitive function, reduces neuronal loss and chronic neuroinflammation, and improves survival after traumatic brain injury …

2019

Background.Xenon is a noble gas with neuroprotective properties. We previously showed that xenon improves short and long-term outcomes in young adult mice after controlled cortical impact (CCI). This is a follow-up study investigating xenon’s effect on very long-term outcome and survival. Methods.C57BL/6N (n=72) young adult male mice received single CCI or sham surgery and were treated with either xenon (75%Xe:25%O2) or control gas (75% N2:25%O2). The outcomes used were: 1) 24-hour lesion volume and neurological outcome score; 2)contextual fear-conditioning at 2 weeks and 20 months; 3) corpus callosum white matter quantification; 4) immunohistological assessment of neuroinflammation and neu…

MaleXenonhippocampusnerve degenerationCorpus callosumBUPRENORPHINEneuroinflammationMice0302 clinical medicineCognition030202 anesthesiologyAnesthesiologyBrain Injuries TraumaticMedicineEPIDEMIOLOGYYoung adultmemory disordersNeuronstraumatic brain injurySham surgeryBrain3. Good healthD-ASPARTATE RECEPTORmedicine.anatomical_structureNeuroprotective AgentsAnesthesianeuroprotectionmedicine.symptomLife Sciences & BiomedicineTraumatic brain injuryHYPOPITUITARISMNeuroprotectionWhite matter03 medical and health sciencesANALGESIAINHALED XENONAnimalsgeneral anaesthesiaSurvival analysisHYPOTHERMIAInflammationScience & Technologybusiness.industry1103 Clinical SciencesHypothermiamedicine.diseaseCOMPETITIVE-INHIBITIONSurvival AnalysisMice Inbred C57BLPATHOLOGYDisease Models AnimalAnesthesiology and Pain MedicineChronic DiseasebusinessCognition Disorders030217 neurology & neurosurgeryWHITE-MATTER DAMAGEFollow-Up StudiesBritish journal of anaesthesia
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Temporal Structure of Human Gaze Dynamics Is Invariant During Free Viewing.

2015

We investigate the dynamic structure of human gaze and present an experimental study of the frequency components of the change in gaze position over time during free viewing of computer-generated fractal images. We show that changes in gaze position are scale-invariant in time with statistical properties that are characteristic of a random walk process. We quantify and track changes in the temporal structure using a well-defined scaling parameter called the Hurst exponent, H. We find H is robust regardless of the spatial complexity generated by the fractal images. In addition, we find the Hurst exponent is invariant across all participants, including those with distinct changes to higher or…

AdultVisual acuityAdolescentEye MovementsComputer scienceInformationSystems_INFORMATIONINTERFACESANDPRESENTATION(e.g.HCI)ComputingMethodologies_IMAGEPROCESSINGANDCOMPUTERVISIONVisual Acuitylcsh:MedicineNeural degenerationTemporal lobeOcular Motility DisordersYoung AdultFractalInformationSystems_MODELSANDPRINCIPLESOcular Motility DisordersMuscle Stretching ExercisesmedicineHumansComputer visionInvariant (mathematics)lcsh:ScienceHurst exponentMultidisciplinarybusiness.industrylcsh:REye movementComputational BiologyRandom walkGazeTemporal LobeFractalsHuman visual system modelNerve Degenerationlcsh:QArtificial intelligencemedicine.symptombusinessResearch ArticlePLoS ONE
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The role of mitochondrial transition pore, and its modulation, in traumatic brain injury and delayed neurodegeneration after TBI

2009

Following severe traumatic brain injury (TBI), a complex interplay of pathomechanism, such as exitotoxicity, oxidative stress, inflammatory events, and mitochondrial dysfunction occurs. This leads to a cascade of neuronal and axonal pathologies, which ultimately lead to axonal failure, neuronal energy metabolic failure, and neuronal death, which in turn determine patient outcome. For mild and moderate TBI, the pathomechanism is similar but much less frequent and ischemic cell death is unusual, except with mass lesions. Involvement of mitochondria in acute post-traumatic neurodegeneration has been extensively studied during the last decade, and there are a number of investigations implicatin…

Time FactorsTraumatic brain injurymedicine.medical_treatmentMitochondrionMitochondrial Membrane Transport ProteinsNeuroprotectionBrain Ischemiachemistry.chemical_compoundDevelopmental NeuroscienceCyclosporin aAnimalsHumansMedicineMitochondrial Permeability Transition Porebusiness.industryMPTPNeurodegenerationmedicine.diseasenervous system diseasesnervous systemNeurologyMitochondrial permeability transition porechemistryBrain InjuriesReperfusion InjuryAcute DiseaseChronic DiseaseNerve DegenerationAxotomybusinessNeuroscience
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The Septum Inguinalis: A Clue to Hernia Genesis?

2018

Purpose: Double ipsilateral inguinal ("pantaloon") hernias and also the more advanced "combined" inguinal hernia involve disruption of the inguinal floor. In the case of pantaloon hernias, the medial boundary of the internal ring remains intact but in combined hernias this is fully disrupted, producing a single hernial protrusion. Deepening the pathophysiology of these hernias may be helpful in addressing hernia genesis, thus improving strategies for the treatment of this disease. Materials and Methods: A cohort of 22 patients who underwent inguinal hernia repair showed double ipsilateral (pantaloon) hernia, comprising distinct direct and indirect protrusions separated by a tissue septum. I…

Malearterial obstructionetiologynerve degenerationInguinal CanalHernia Inguinalhernia03 medical and health sciences0302 clinical medicineTissue markersmedicineHumansHerniaHerniorrhaphyAgedAged 80 and overNerve degenerationbusiness.industryAbdominal WallInguinal herniamuscle degenerationMuscle degenerationAnatomyArterial obstructionMiddle Agedmedicine.diseasedigestive system diseasesseptum inguinalisstomatognathic diseasesInguinal herniasurgical procedures operativemedicine.anatomical_structure030220 oncology & carcinogenesisFemale030211 gastroenterology & hepatologySurgerybusinessInferior epigastric vessels
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Polyglutamine toxicity induces rod photoreceptor division, morphological transformation or death in Spinocerebellar ataxia 7 mouse retina

2010

In neurodegenerative disorders caused by polyglutamine (polyQ) expansion, polyQ toxicity is thought to trigger a linear cascade of successive degenerative events leading to neuronal death. To understand how neurons cope with polyQ toxicity, we studied a Spinocerebellar ataxia 7 (SCA7) mouse which expresses polyQ-expanded ATXN7 only in rod photoreceptors. We show that in response to polyQ toxicity, SCA7 rods go through a range of radically different cell fates, including apoptotic and non-apoptotic cell death, cell migration, morphological transformation into a round cell or, most remarkably, cell division. The temporal profile of retinal remodeling indicates that some degenerative pathways …

Programmed cell deathCell divisionProliferationPopulationMice TransgenicNerve Tissue ProteinsBiologylcsh:RC321-571Mice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell MovementRetinal Rod Photoreceptor CellsmedicineAnimalsSpinocerebellar AtaxiasNeurodegenerationeducationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryCell ShapeComputingMilieux_MISCELLANEOUSSpinocerebellar ataxia 7030304 developmental biologyAtaxin-7Mice Knockout0303 health sciencesRetinaeducation.field_of_studyPhotoreceptorCell DeathRetinal DegenerationNeurodegenerationRetinalmedicine.diseaseRemodelingMice Inbred C57BLmedicine.anatomical_structureNeurologyProteotoxicitychemistryNerve DegenerationSpinocerebellar ataxia[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Apoptosis Regulatory ProteinsPeptidesPolyglutamineNeuroscience030217 neurology & neurosurgery
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PGC-1α: a master gene that is hard to master

2012

Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is a transcriptional coactivator that favorably affects mitochondrial function. This concept is supported by an increasing amount of data including studies in PGC-1α gene-deleted mice, suggesting that PGC-1α is a rescue factor capable of boosting cell metabolism and promoting cell survival. However, this view has now been called into question by a recent study showing that adeno-associated virus-mediated PGC-1α overexpression causes overt cell degeneration in dopaminergic neurons. How is this to be understood, and can these seemingly conflicting findings tell us something about the role of PGC-1α in cell stress and in cont…

medicine.medical_specialtyModels NeurologicalSettore BIO/11 - Biologia MolecolareRNA-binding proteinBiologyMitochondrionSettore BIO/09 - FisiologiaMiceCellular and Molecular NeuroscienceHeat shock proteinInternal medicinemedicineAnimalsHomeostasisHumansReceptorMolecular BiologyTranscription factorHeat-Shock ProteinsMice KnockoutPharmacologyPGC-1α Mitochondria Dopaminergic neurons Transgenic animal Adenovirus Parkinson’s diseaseDopaminergic NeuronsDopaminergicRNA-Binding ProteinsParkinson DiseaseCell BiologyPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMitochondriaEndocrinologyCell metabolismNerve DegenerationTrans-ActivatorsMolecular MedicineNeuroscienceHomeostasisTranscription FactorsCellular and Molecular Life Sciences
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Loss of input from the mossy cells blocks maturation of newly generated granule cells.

2007

The objective of this work is to check whether the input from the mossy cells to the inner molecular layer is necessary for the integration and maturation of the newly generated granule cells of the dentate gyrus (DG) in mice, and if after status epilepticus the sprouting of the mossy fibers can substitute for this projection. Newly generated cells were labeled by administration of 5-bromo-deoxyuridine either before or after pilocarpine administration. The neuronal loss in the hippocampus after administration of pilocarpine combined with scopolamine and diazepam seemed restricted to the hilar mossy cells. The maturation of the granule cells was studied using immunohistochemistry for calreti…

Cell typeCell SurvivalCognitive NeuroscienceScopolamineConvulsantsNerve Tissue ProteinsMuscarinic Antagonistschemistry.chemical_compoundMiceS100 Calcium Binding Protein GStatus EpilepticusmedicineAnimalsCell ProliferationDiazepamEpilepsyNeuronal PlasticitybiologyChemistryDentate gyrusStem CellsGranule (cell biology)PilocarpineNuclear ProteinsCell DifferentiationImmunohistochemistryDNA-Binding Proteinsnervous systemBromodeoxyuridinePilocarpineCalbindin 2Dentate GyrusMossy Fibers HippocampalNerve Degenerationbiology.proteinAnticonvulsantsFemaleNeuNCalretininNeuroscienceBromodeoxyuridineBiomarkersSproutingmedicine.drugHippocampus
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