Search results for "Juries"

showing 10 items of 639 documents

Dimethyl fumarate treatment after traumatic brain injury prevents depletion of antioxidative brain glutathione and confers neuroprotection.

2017

Dimethyl fumarate (DMF) is an immunomodulatory compound to treat multiple sclerosis and psoriasis with neuroprotective potential. Its mechanism of action involves activation of the antioxidant pathway regulator Nuclear factor erythroid 2-related factor 2 thereby increasing synthesis of the cellular antioxidant glutathione (GSH). The objective of this study was to investigate whether post-traumatic DMF treatment is beneficial after experimental traumatic brain injury (TBI). Adult C57Bl/6 mice were subjected to controlled cortical impact followed by oral administration of DMF (80 mg/kg body weight) or vehicle at 3, 24, 48, and 72 h after the inflicted TBI. At 4 days after lesion (dal), DMF-tr…

0301 basic medicineMaleTraumatic brain injuryDimethyl FumarateBrain damagePharmacologyBlood–brain barrierBiochemistryNeuroprotectionAntioxidantsLesion03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineBrain Injuries TraumaticmedicineAnimalsNeuroinflammationDimethyl fumarateGlutathionemedicine.diseaseGlutathioneNeuroprotectionMice Inbred C57BLDisease Models AnimalOxidative Stress030104 developmental biologymedicine.anatomical_structureNeuroprotective AgentsBiochemistrychemistryBlood-Brain Barriermedicine.symptom030217 neurology & neurosurgeryJournal of neurochemistry
researchProduct

Proinflammatory and amyloidogenic S100A9 induced by traumatic brain injury in mouse model.

2019

Traumatic brain injury (TBI) represents a significant risk factor for development of neurodegenerative diseases such as Alzheimer’s and Parkinson’s. The S100A9-driven amyloid-neuroinflammatory cascade occurring during primary and secondary TBI events can serve as a mechanistic link between TBI and Alzheimer’s as demonstrated recently in the human brain tissues. Here by using immunohistochemistry in the controlled cortical impact TBI mouse model we have found pro-inflammatory S100A9 in the brain tissues of all mice on the first and third post-TBI days, while 70% of mice did not show any S100A9 presence on seventh post-TBI day similar to controls. This indicates that defensive mechanisms effe…

0301 basic medicineMalemedicine.medical_specialtyNeurologyAmyloidTraumatic brain injuryPlaque AmyloidProtein Aggregation PathologicalS100A9Proinflammatory cytokine03 medical and health sciencesMice0302 clinical medicineBrain Injuries TraumaticmedicineAnimalsCalgranulin BSignificant riskNeuroinflammationNeuronsbusiness.industryGeneral NeuroscienceBrainmedicine.diseasenervous system diseasesDisease Models Animal030104 developmental biologyMicrogliabusinessAlzheimer’s disease Amyloid Neuroinflammation Oligomerization S100A9 Traumatic brain injuryNeuroscience030217 neurology & neurosurgeryNeuroscience letters
researchProduct

Sex hormones modulate pathogenic processes in experimental traumatic brain injury.

2018

Clinical and animal studies have revealed sex-specific differences in histopathological and neurological outcome after traumatic brain injury (TBI). The impact of perioperative administration of sex steroid inhibitors on TBI is still elusive. Here, we subjected male and female C57Bl/6N mice to the controlled cortical impact (CCI) model of TBI and applied pharmacological inhibitors of steroid hormone synthesis, that is, letrozole (LET, inhibiting estradiol synthesis by aromatase) and finasteride (FIN, inhibiting dihydrotestosterone synthesis by 5α-reductase), respectively, starting 72 h prior CCI, and continuing for a further 48 h after CCI. Initial gene expression analyses showed that andro…

0301 basic medicineMalemedicine.medical_specialtyanimal structuresmedicine.drug_classmedicine.medical_treatmentTropomyosin receptor kinase BTropomyosin receptor kinase ABiochemistryNeuroprotection03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineInternal medicineBrain Injuries TraumaticmedicineAnimalsNerve Growth FactorsSex CharacteristicsbiologyEstradiolbusiness.industryEstrogen AntagonistsBrainDihydrotestosteroneAndrogennervous system diseasesMice Inbred C57BLSteroid hormoneDisease Models Animal030104 developmental biologyEndocrinologynervous systemSex steroidDihydrotestosteronebiology.proteinFemalebusiness030217 neurology & neurosurgeryNeurotrophinmedicine.drugJournal of neurochemistry
researchProduct

Profilin 1 delivery tunes cytoskeletal dynamics toward CNS axon regeneration

2020

After trauma, regeneration of adult CNS axons is abortive, causing devastating neurologic deficits. Despite progress in rehabilitative care, there is no effective treatment that stimulates axonal growth following injury. Using models with different regenerative capacities, followed by gain- and loss-of-function analysis, we identified profilin 1 (Pfn1) as a coordinator of actin and microtubules (MTs), powering axonal growth and regeneration. In growth cones, Pfn1 increased actin retrograde flow, MT growth speed, and invasion of filopodia by MTs, orchestrating cytoskeletal dynamics toward axonal growth. In vitro, active Pfn1 promoted MT growth in a formin-dependent manner, whereas localizati…

0301 basic medicineNervous systemGrowth ConesNeuromuscular Junctionmacromolecular substancesGlial scar03 medical and health sciencesMiceProfilins0302 clinical medicineTransduction GeneticmedicineAnimalsAxonGrowth coneCytoskeletonSpinal Cord InjuriesMice KnockoutbiologyRegeneration (biology)General MedicineGenetic TherapyDependovirusSciatic NerveCell biologyNerve Regeneration030104 developmental biologymedicine.anatomical_structurenervous system030220 oncology & carcinogenesisForminsbiology.proteinSciatic nerveFilopodiaResearch Article
researchProduct

Loss of synaptic zinc transport in progranulin deficient mice may contribute to progranulin-associated psychopathology and chronic pain

2017

Affective and cognitive processing of nociception contributes to the development of chronic pain and vice versa, pain may precipitate psychopathologic symptoms. We hypothesized a higher risk for the latter with immanent neurologic diseases and studied this potential interrelationship in progranulin-deficient mice, which are a model for frontotemporal dementia, a disease dominated by behavioral abnormalities in humans. Young naïve progranulin deficient mice behaved normal in tests of short-term memory, anxiety, depression and nociception, but after peripheral nerve injury, they showed attention-deficit and depression-like behavior, over-activity, loss of shelter-seeking, reduced impulse cont…

0301 basic medicineNeurotransmitter transportermedicine.medical_specialtyMice03 medical and health sciencesProgranulins0302 clinical medicinePeripheral Nerve InjuriesInternal medicinemental disordersmedicineAnimalsPrefrontal cortexMolecular BiologyGranulinsMice KnockoutIon Transportbusiness.industryChronic painmedicine.diseaseZinc030104 developmental biologyNociceptionEndocrinologyCompulsive behaviorNeuropathic painPeripheral nerve injuryIntercellular Signaling Peptides and ProteinsNeuralgiaMolecular MedicineChronic Painmedicine.symptomCarrier Proteinsbusiness030217 neurology & neurosurgeryFrontotemporal dementiaBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
researchProduct

Acute Cortical Transhemispheric Diaschisis after Unilateral Traumatic Brain Injury

2017

Focal neocortical brain injuries lead to functional alterations, which can spread beyond lesion-neighboring brain areas. The undamaged hemisphere and its associated disturbances after a unilateral lesion, so-called transhemispheric diaschisis, have been progressively disclosed over the last decades; they are strongly involved in the pathophysiology and, potentially, recovery of brain injuries. Understanding the temporal dynamics of these transhemispheric functional changes is crucial to decipher the role of the undamaged cortex in the processes of functional reorganization at different stages post-lesion. In this regard, little is known about the acute-subacute processes after 24-48 h in th…

0301 basic medicinePatch-Clamp TechniquesTraumatic brain injurySomatosensory system03 medical and health sciences0302 clinical medicineCortex (anatomy)Unilateral lesionBrain Injuries TraumaticNeuroplasticitymedicineAnimalsDiaschisisNeuronal PlasticityMotor CortexElectroencephalographySomatosensory Cortexmedicine.diseaseMice Inbred C57BLDisease Models AnimalElectrophysiology030104 developmental biologymedicine.anatomical_structureBrain HemisphereNeurology (clinical)PsychologyNeuroscience030217 neurology & neurosurgeryJournal of Neurotrauma
researchProduct

Introducing the concept of “CSF-shift edema” in traumatic brain injury

2018

Brain edema after severe traumatic brain injury (TBI) plays an important role in the outcome and survival of injured patients. It is also one of the main targets in the therapeutic approach in the current clinical practice. To date, the pathophysiology of traumatic brain swelling is complex and, being that it is thought to be mainly cytotoxic and vasogenic in origin, not yet entirely understood. However, based on new understandings of the hydrodynamic aspects of cerebrospinal fluid (CSF), an additional mechanism of brain swelling can be considered. An increase in pressure into the subarachnoid space, secondary to traumatic subarachnoid hemorrhage, would result in a rapid shift of CSF from t…

0301 basic medicinePathologymedicine.medical_specialtySubarachnoid hemorrhageTraumatic brain injurybrain edema; cisternostomy; decompressive hemicraniectomy; paravascular pathway; traumatic brain injury; Cellular and Molecular NeuroscienceBrain water03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineCerebrospinal fluidEdemaBrain Injuries TraumaticmedicineHumansparavascular pathwaybrain edemaBrain edemabusiness.industrytraumatic brain injurymedicine.diseasecisternostomyPathophysiology030104 developmental biologymedicine.anatomical_structureSubarachnoid spacemedicine.symptomExtracellular Spacebusinessdecompressive hemicraniectomybrain edema; cisternostomy; decompressive hemicraniectomy; paravascular pathway; traumatic brain injury030217 neurology & neurosurgeryJournal of Neuroscience Research
researchProduct

Irreversible changes occurring in long-term denervated Schwann cells affect delayed nerve repair.

2017

OBJECTIVEMultiple factors may affect functional recovery after peripheral nerve injury, among them the lesion site and the interval between the injury and the surgical repair. When the nerve segment distal to the lesion site undergoes chronic degeneration, the ensuing regeneration (when allowed) is often poor. The aims of the current study were as follows: 1) to examine the expression changes of the neuregulin 1/ErbB system during long-term nerve degeneration; and 2) to investigate whether a chronically denervated distal nerve stump can sustain nerve regeneration of freshly axotomized axons.METHODSThis study used a rat surgical model of delayed nerve repair consisting of a cross suture betw…

0301 basic medicinePathologymedicine.medical_specialtyTime FactorsNerve rootNeuregulin-1Settore MED/19 - Chirurgia PlasticaSchwann cellNRG1/ErbB system03 medical and health sciences0302 clinical medicinePeripheral Nerve InjuriesMedicineAnimalsNeuregulin 1Rats Wistardelayed nerve repairDenervationneuregulin 1biologybusiness.industryRegeneration (biology)General MedicineAnatomyRecovery of FunctionDenervationMedian nerveNerve RegenerationRats030104 developmental biologymedicine.anatomical_structureperipheral nervePeripheral nerve injuryNerve Degenerationstereologybiology.proteinFemaleSchwann CellsbusinessEpineurial repair030217 neurology & neurosurgeryJournal of neurosurgery
researchProduct

Cold Atmospheric Plasma Promotes Regeneration-Associated Cell Functions of Murine Cementoblasts In Vitro

2021

The aim of the study was to examine the efficacy of cold atmospheric plasma (CAP) on the mineralization and cell proliferation of murine dental cementoblasts. Cells were treated with CAP and enamel matrix derivates (EMD). Gene expression of alkaline phosphatase (ALP), bone gamma-carboxyglutamate protein (BGLAP), periostin (POSTN), osteopontin (OPN), osterix (OSX), collagen type I alpha 1 chain (COL1A1), dentin matrix acidic phosphoprotein (DMP)1, RUNX family transcription factor (RUNX)2, and marker of proliferation Ki-67 (KI67) was quantified by real-time PCR. Protein expression was analyzed by immunocytochemistry and ELISA. ALP activity was determined by ALP assay. Von Kossa and alizarin r…

0301 basic medicinePlasma GasesGene Expressioncold atmospheric plasmaMice0302 clinical medicineCell MovementmineralizationOsteopontinBiology (General)CementogenesisSpectroscopyDental CementumbiologyChemistryCell DifferentiationGeneral Medicinetraumatic dental injuriesdental hard tissue regeneration therapyComputer Science ApplicationsChemistryAlkaline phosphatasecementoblastsemdogainQH301-705.5Cell SurvivalproliferationCementoblastOsteocalcinPeriostinArticleCatalysisCell LineInorganic Chemistry03 medical and health sciencesCalcification Physiologicstomatognathic systemAnimalsViability assayPhysical and Theoretical ChemistryQD1-999Molecular BiologyCell ProliferationCell growthOrganic Chemistry030206 dentistryMolecular biologyDMP1Collagen type I alpha 1030104 developmental biologyGene Expression Regulationbiology.proteinOsteopontinTranscriptomeInternational Journal of Molecular Sciences
researchProduct

Peroxisome proliferator-activated receptor-γ coactivator-1α mediates neuroprotection against excitotoxic brain injury in transgenic mice: role of mit…

2016

Peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) is a transcriptional coactivator involved in the regulation of mitochondrial biogenesis and cell defense. The functions of PGC-1α in physiology of brain mitochondria are, however, not fully understood. To address this we have studied wild-type and transgenic mice with a two-fold overexpression of PGC-1α in brain neurons. Data showed that the relative number and basal respiration of brain mitochondria were increased in PGC-1α transgenic mice compared with wild-type mitochondria. These changes occurred concomitantly with altered levels of proteins involved in oxidative phosphorylation (OXPHOS) as studied by proteomi…

0301 basic medicineProgrammed cell deathKainic acidTransgenebcl-X ProteinPeroxisome proliferator-activated receptorBiologyInhibitor of apoptosisSettore BIO/09 - FisiologiaNeuroprotectionOxidative PhosphorylationInhibitor of Apoptosis ProteinsMice03 medical and health scienceschemistry.chemical_compoundXIAP0302 clinical medicineBrain InjurieInhibitor of Apoptosis ProteinAnimalsCA1 Region HippocampalCells CulturedNeuronschemistry.chemical_classificationNeuroscience (all)Kainic AcidCell DeathAnimalNeuron survivalGeneral NeuroscienceProteomicXIAP; Kainic acid; Mitochondria; Neuron survival; PGC-1α; Proteomics; Animals; Brain Injuries; CA1 Region Hippocampal; Cell Death; Cells Cultured; Inhibitor of Apoptosis Proteins; Kainic Acid; Mice; Mitochondria; Neurons; Oxidative Phosphorylation; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; Proto-Oncogene Proteins c-bcl-2; bcl-X Protein; Neuroscience (all)NeuronPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMitochondriaCell biologyXIAP030104 developmental biologyProto-Oncogene Proteins c-bcl-2chemistryMitochondrial biogenesisBrain InjuriesImmunologyPGC-1α030217 neurology & neurosurgeryEuropean Journal of Neuroscience
researchProduct