Search results for "DEGENERATION"

showing 10 items of 601 documents

Cannabinoid CB1 receptors regulate neuronal TNF-α effects in experimental autoimmune encephalomyelitis.

2011

Abstract Cannabinoid CB1 receptors (CB1Rs) regulate the neurodegenerative damage of experimental autoimmune encephalomyelitis (EAE) and of multiple sclerosis (MS). The mechanism by which CB1R stimulation exerts protective effects is still unclear. Here we show that pharmacological activation of CB1Rs dampens the tumor necrosis factor α (TNFα)-mediated potentiation of striatal spontaneous glutamate-mediated excitatory postsynaptic currents (EPSCs), which is believed to cogently contribute to the inflammation-induced neurodegenerative damage observed in EAE mice. Furthermore, mice lacking CB1Rs showed a more severe clinical course and, in parallel, exacerbated alterations of sEPSC duration af…

Cannabinoid receptorEncephalomyelitis Autoimmune ExperimentalPolyunsaturated Alkamidesmedicine.medical_treatmentImmunologyExcitotoxicityGlutamic AcidArachidonic AcidsPharmacologyBiologymedicine.disease_causeReceptors N-Methyl-D-AspartateReceptors Tumor Necrosis FactorAmidohydrolasesEtanerceptBehavioral Neurosciencechemistry.chemical_compoundMiceReceptor Cannabinoid CB1Fatty acid amide hydrolaseCannabinoid Receptor ModulatorsmedicineAnimalsDronabinolReceptors AMPA6-Cyano-7-nitroquinoxaline-23-dioneMice KnockoutNeuronsEndocrine and Autonomic SystemsTumor Necrosis Factor-alphaNeurodegenerationExperimental autoimmune encephalomyelitisExcitatory Postsynaptic PotentialsAnandamidemedicine.diseaseEndocannabinoid systemCorpus StriatumMice Inbred C57BLchemistryImmunoglobulin GImmunologyNerve DegenerationSettore MED/26 - NeurologiaFemaleCannabinoidDizocilpine MaleateEndocannabinoidsBrain, behavior, and immunity
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A Case of Follicular Tumor of Uncertain Malignant Potential (FT-UMP) with Glomeruloid Features Showing Capsular Mucinous Degeneration

2021

The most recent revision of the World Health Organization (WHO) Classification of Tumours of Endocrine Organs introduced a new variant of follicular thyroid carcinoma (FTC). It is characterized by a “glomeruloid” architectural pattern of growth. We present a case of follicular tumor with glomeruloid features, with Alcian Blue positive mucinous stromal degeneration in foci of questionable capsular microinvasion. At our knowledge, this the second case of glomeruloid follicular tumor in the literature and the first case in which Alcian Blue staining was used to investigate capsular invasion. Moreover, RAS mutation further supports that this is a variant of follicular tumor with uncertain malig…

Capsular InvasionPathologymedicine.medical_specialtyendocrine systemStromal cell030209 endocrinology & metabolismCase ReportSettore MED/08 - Anatomia PatologicaMucinous degenerationWorld healthThyroid carcinomaGlomeruloid Features03 medical and health sciences0302 clinical medicineFollicular phasemedicinePathologyEndocrine systemRB1-214Follicular Tumor of Uncertain Malignant Potential (FT-UMP)business.industryGeneral MedicineStainingSettore MED/18 - Chirurgia Generale030220 oncology & carcinogenesisbusinessCase Reports in Pathology
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Characterization of the cortical laser-doppler flow and hippocampal degenerative patterns after global cerebral ischaemia in the goat.

1998

Large-animal models offer several advantages in the study of cerebral ischaemia: easier control of physiological variables, easier neuropathological evaluation, etc. In the present study we have taken advantage of the unique cerebrovascular anatomy of the goat to reproduce a model of reversible, incomplete, global cerebral ischaemia in a large-sized animal species, in which the effects of successive manoeuvres to stop and re-start cerebral blood flow can be recorded continuously. Early cortical laser-Doppler flow response (up to 2 h) and delayed neuronal degeneration (7 days) in the hippocampal CA1 subfield have been analysed in goats undergoing 5, 10 or 20 min of transient, global cerebral…

Carotid Artery DiseasesTime FactorsPhysiologyClinical BiochemistryExternal carotid arteryIschemiaArterial Occlusive DiseasesHyperemiaHippocampusHyperaemiaPhysiology (medical)medicine.arteryOcclusionmedicineLaser-Doppler FlowmetryAnimalsIntracranial pressureCell Deathbusiness.industryGoatsPyramidal CellsHemodynamicsElectroencephalographymedicine.diseaseBlood pressureCerebral blood flowIschemic Attack TransientAnesthesiaCerebrovascular CirculationNerve DegenerationReperfusionFemalemedicine.symptombusinessPerfusionPflugers Archiv : European journal of physiology
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Chondrodysplasia punctata — Rhizomelic form

1976

Pathologic, ultrastructural and radiologic studies are described on 3 infants with the rhizomelic form of chondrodysplasia punctata. Radiologic criteria in the young infant include radiolucent coronal clefts dividing all or most of the thoracic and lumbar vertebral bodies, short humeri with flared metaphyses and punctate calcifications commonly present adjacent to the ossified ischial and pubic bones and less commonly in other locations. In late infancy and childhood the radiologic criteria include demineralization in all bones with slow maturation, flat vertebral bodies, short humeri and femora, metaphyseal flaring, especially in the distal humerus, proximal femur and proximal tibia, immat…

Cartilage ArticularMalemusculoskeletal diseasesChondrodysplasia PunctataPathologymedicine.medical_specialtyContractureDegeneration (medical)Skin DiseasesBone and BonesCataractInfant Newborn DiseasesLumbarmedicineHumansChondrodysplasia punctataFemurChildPelvisCerebral CortexNeuronsbusiness.industryCartilageMetaphyseal flaringInfant NewbornInfantPatellaAnatomyHumerusCystic Changemedicine.diseaseCartilagemedicine.anatomical_structureChild PreschoolPediatrics Perinatology and Child HealthMicrocephalyFemalePsychomotor DisordersbusinessCancellous boneEuropean Journal of Pediatrics
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Membrane protein oxidation determines neuronal degeneration

2015

Oxidative stress is an early hallmark in neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. However, the critical biochemical effector mechanisms of oxidative neurotoxicity have remained surprisingly elusive. In screening various peroxides and potential substrates of oxidation for their effect on neuronal survival, we observed that intramembrane compounds were significantly more active than aqueous or amphiphilic compounds. To better understand this result, we synthesized a series of competitive and site-specific membrane protein oxidation inhibitors termed aminoacyllipids, whose structures were designed on the basis of amino acids frequently found at the protein-lipi…

Cell SurvivalBiologyProtein oxidationmedicine.disease_causeBiochemistryProtein Structure SecondaryRats Sprague-DawleyCellular and Molecular Neurosciencechemistry.chemical_compoundmedicineAnimalsLipid bilayerCells CulturedNeuronsSphingosineNeurodegenerationNeurotoxicityMembrane Proteinsmedicine.diseaseTransmembrane proteinRatsCell biologyOxidative StressMembrane proteinchemistryNerve DegenerationReactive Oxygen SpeciesOxidation-ReductionOxidative stressJournal of Neurochemistry
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Central and Peripheral Secondary Cell Death Processes after Transient Global Ischemia in Nonhuman Primate Cerebellum and Heart

2019

Cerebral ischemia and its pathological sequelae are responsible for severe neurological deficits generally attributed to the neural death within the infarcted tissue and adjacent regions. Distal brain regions, and even peripheral organs, may be subject to more subtle consequences of the primary ischemic event which can initiate parallel disease processes and promote comorbid symptomology. In order to characterize the susceptibility of cerebellar brain regions and the heart to transient global ischemia (TGI) in nonhuman primates (NHP), brain and heart tissues were harvested 6 months post-TGI injury. Immunostaining analysis with unbiased stereology revealed significant cell death in lobule II…

Cell deathInflammationPathologymedicine.medical_specialtyProgrammed cell deathCerebellumbusiness.industryPurkinje cellNeurodegenerationIschemiaInflammationStereologymedicine.diseaseSecondary injury03 medical and health sciences0302 clinical medicinemedicine.anatomical_structureApoptosis030220 oncology & carcinogenesisMedicineNeurodegenerationmedicine.symptombusiness030217 neurology & neurosurgeryImmunostaining
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An unconventional role for miRNA: let-7 activates Toll-like receptor 7 and causes neurodegeneration

2011

Activation of innate immune receptors by host-derived factors exacerbates CNS damage, but the identity of these factors remains elusive. We uncovered an unconventional role for the microRNA let-7, a highly abundant regulator of gene expression in the CNS, in which extracellular let-7 activates the RNA-sensing Toll-like receptor (TLR) 7 and induces neurodegeneration through neuronal TLR7. Cerebrospinal fluid (CSF) from individuals with Alzheimer’s disease contains increased amounts of let-7b, and extracellular introduction of let-7b into the CSF of wild-type mice by intrathecal injection resulted in neurodegeneration. Mice lacking TLR7 were resistant to this neurodegenerative effect, but thi…

Cell signalingApoptosisElectrophoretic Mobility Shift AssayBiologyReal-Time Polymerase Chain ReactionMiceAlzheimer DiseasemicroRNAExtracellularmedicineAnimalsHumansReceptorIn Situ HybridizationMice KnockoutNeuronsToll-like receptorMembrane GlycoproteinsMicroscopy ConfocalInnate immune systemGeneral NeuroscienceNeurodegenerationBrainvirus diseasesTLR7medicine.diseaseImmunohistochemistryMice Inbred C57BLMicroRNAsHEK293 CellsToll-Like Receptor 7Nerve DegenerationCancer researchSignal TransductionNature Neuroscience
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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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Marklose nervenfasern im Senium und im Sp�tstadium der Thalidomid-Polyneuropathie: quantitativ-elektronenmikroskopische Untersuchungen

1977

Sural nerve biopsies of four patients, aged 54–76 years, with a predominantly sensory type of neuropathy following high dosages of thalidomide were examined by light and electron microscopy. The present study includes a qualitative and quantitative evaluation of unmyelinated nerve fibers. Despite severe neuropathy, increased numbers of small unmyelinated axons per endoncurial area were noted in all patients. This numerical increase appeared to be independent of aging, since it was not seen in two senile controls, studied at the age of 83 and 88 years. The increase in the endoneurial density of unmyelinated axons, especially of small sized fibers, is likely to be related to regeneration foll…

Cellular and Molecular Neurosciencenervous systembusiness.industryUnmyelinated nerve fiberSensory neuropathyMedicineSural nerveNeurology (clinical)Degeneration (medical)AnatomybusinessPathology and Forensic MedicineActa Neuropathologica
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Involvement of Kv3.1 potassium chanels in 7-ketocholesterol, 24S-hydroxycholesterol and C24 : 0-induced lipotoxicity on 158N and BV-2 cells : relatio…

2017

Potassium (K+) is involved in the regulation of cellular excitability, cell cycle regulation, cell viability, neuroprotection and maintenance of microglial and oligodendrocytic functions. Potassium dysfunction, described in several neurodegenerative diseases such as Alzheimer's Disease (AD), multiple sclerosis (MS), Parkinson's disease and Huntington's disease, may be a potential therapeutic target. The underlying toxic mechanisms of these neurodegenerative pathologies involve oxysterols, which are oxidized cholesterol derivatives, and fatty acids including those associated with peroxisomal metabolism. 7-ketocholesterol (7KC), 24S-hydroxycholesterol (24S-OHC) and tetracosanoic acid (C24:0),…

Cellules microgliales murines BV-2Oligodengrocytes murins 158N158N murine oligodendrocytesCanaux KvKv3.1b7-cétocholestérolNeurodégénérescenceMaladie d’Alzheimer24S-hydroxycholesterolTetracosanoic acid (C24:0)24S-hydroxycholestérolPotassium[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAcide tétracosanoïque (C24:0)NeurodegenerationMurine microglial BV-2 cellsAlzheimer’s disease7-ketocholesterolKv channels
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