Search results for "trauma"

showing 10 items of 848 documents

Treatment with albumin-hydroxyoleic acid complex restores sensorimotor function in rats with spinal cord injury: Efficacy and gene expression regulat…

2017

Sensorimotor dysfunction following incomplete spinal cord injury (SCI) is often characterized by paralysis, spasticity and pain. Previously, we showed that intrathecal (i.t.) administration of the albumin-oleic acid (A-OA) complex in rats with SCI produced partial improvement of these symptoms and that oral 2-hydroxyoleic acid (HOA, a non-hydrolyzable OA analogue), was efficacious in the modulation and treatment of nociception and pain-related anxiety, respectively. Here we observed that intrathecal treatment with the complex albumin-HOA (A-HOA) every 3 days following T9 spinal contusion injury improved locomotor function assessed with the Rotarod and inhibited TA noxious reflex activity in…

0301 basic medicineMaleNociceptionCritical Care and Emergency Medicinelcsh:MedicineGene ExpressionOleic AcidsPharmacologyProstaglandin E synthaseImmune ReceptorsBiochemistry0302 clinical medicineCell SignalingMedicine and Health SciencesMembrane Receptor Signalinglcsh:ScienceSpinal Cord InjurySpinal cord injuryToll-like ReceptorsTrauma MedicineInjections SpinalProstaglandin-E SynthasesExtracellular Matrix ProteinsMultidisciplinaryImmune System ProteinsbiologyTenascin CTenascinComplement ReceptorsImmune Receptor SignalingNociceptionTreatment OutcomeNeurologySpinal CordPhospholipasesmedicine.symptomTraumatic InjuryLocomotionResearch ArticleSignal TransductionTransmembrane ReceptorsImmunologyPainInflammationNerve Tissue ProteinsGrowth Differentiation Factor 10Drug Administration Schedule03 medical and health sciencesAlbuminsmedicineGeneticsAnimalsParalysisSpasticityRats WistarSpinal Cord Injuriesbusiness.industrylcsh:RBiology and Life SciencesProteinsCell BiologyRecovery of Functionmedicine.diseaseNeuroregenerationRats030104 developmental biologyGene Expression RegulationGDF10Rotarod Performance Testbiology.proteinlcsh:QbusinessNeurotrauma030217 neurology & neurosurgeryPLoS ONE
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Short‐term neuropsychiatric outcomes and quality of life in COVID‐19 survivors

2021

BACKGROUND: The general medical impacts of coronavirus (COVID-19) are increasingly appreciated. However, its impact on neurocognitive, psychiatric health and quality of life (QoL) in survivors after the acute phase is poorly understood. We aimed to evaluate neurocognitive function, psychiatric symptoms, and QoL in COVID-19 survivors shortly after hospital discharge. METHODS: This was a cross-sectional analysis of a prospective study of hospitalised COVID-19 survivors followed-up for 2 months after discharge. A battery of standardised instruments evaluating neurocognitive function, psychiatric morbidity, and QoL (mental and physical components) was administered by telephone. RESULTS: Of the …

0301 basic medicineMalePediatrics030204 cardiovascular system & hematologyAnxietySevere Acute Respiratory SyndromeStress Disorders Post-Traumatic0302 clinical medicineCognitionQuality of lifeOutcome Assessment Health CareMedicineVerbal fluency testProspective StudiesSurvivorsProspective cohort studyLetter to the EditorDepression (differential diagnoses)Aged 80 and overPsychiatryDepressionMiddle AgedsequelaehumanitiesMemory Short-TermneurocognitiveAnxietyFemaleOriginal Articlemedicine.symptomAdultmedicine.medical_specialtypsychiatric morbidity03 medical and health sciencesYoung AdultSex FactorsCOVID‐19Internal MedicineHumansAgedMemory Disordersbusiness.industryWorking memorySARS-CoV-2COVID-19Original Articles030104 developmental biologyCross-Sectional Studiesquality of lifeDeliriumbusinessCognition DisordersNeurocognitiveCOVID-19 neurocognitive psychiatric morbidity quality of life sequelaeJournal of Internal Medicine
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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
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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
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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
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Formin 2 links neuropsychiatric phenotypes at young age to an increased risk for dementia

2017

Age-associated memory decline is due to variable combinations of genetic and environmental risk factors. How these risk factors interact to drive disease onset is currently unknown. Here we begin to elucidate the mechanisms by which post-traumatic stress disorder (PTSD) at a young age contributes to an increased risk to develop dementia at old age. We show that the actin nucleator Formin 2 (Fmn2) is deregulated in PTSD and in Alzheimer's disease (AD) patients. Young mice lacking the Fmn2 gene exhibit PTSD-like phenotypes and corresponding impairments of synaptic plasticity, while the consolidation of new memories is unaffected. However, Fmn2 mutant mice develop accelerated age-associated me…

0301 basic medicineMalememoriaAginggenetics [Stress Disorders Post-Traumatic]Diseasegenetics [Neuronal Plasticity]BioinformaticsdemenciaStress Disorders Post-TraumaticMice0302 clinical medicineRisk FactorsNews & ViewsAge of OnsetMice KnockoutNeuronal PlasticitybiologyGeneral NeuroscienceMicrofilament ProteinsNuclear Proteinsgenetics [Nuclear Proteins]FearadultoMiddle AgedAlzheimer's diseasephysiology [Aging]Phenotype3. Good healthPhenotypemiedoFormin 2Forminsgenetics [Aging]estres postraumaticoepidemiology [Stress Disorders Post-Traumatic]AdultHDAC inhibidorpsychology [Dementia]alzheimerForminsNerve Tissue Proteinsepidemiology [Dementia]Affect (psychology)General Biochemistry Genetics and Molecular Biology03 medical and health sciencesHDAC inhibitorMemorygenetics [Dementia]ddc:570medicineDementiaAnimalsHumansenvejecimientoMolecular Biologyphysiology [Memory]General Immunology and MicrobiologyPost-traumatic stress disordermedicine.diseaseYoung age030104 developmental biologyformin 2 protein mouseCase-Control StudiesSynaptic plasticitybiology.proteinDementiagenetics [Microfilament Proteins]complications [Stress Disorders Post-Traumatic]030217 neurology & neurosurgeryHomeostasis
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An update on intracerebral stem cell grafts.

2018

Introduction: Primary neurological disorders are notoriously debilitating and deadly, and over the past four decades stem cell therapy has emerged as a promising treatment. Translation of stem cell therapies from the bench to the clinic requires a better understanding of delivery protocols, safety profile, and efficacy in each disease. Areas covered: In this review, benefits and risks of intracerebral stem cell transplantation are presented for consideration. Milestone discoveries in stem cell applications are reviewed to examine the efficacy and safety of intracerebral stem cell transplant therapy for disorders of the central nervous system and inform design of translatable protocols for c…

0301 basic medicineOncologymedicine.medical_specialtyParkinson's diseaseTraumatic brain injurymedicine.medical_treatmentmulti-system atrophyNeuroprotection03 medical and health sciencesGraft vs Host Reaction0302 clinical medicineHuntington's diseaseCentral Nervous System DiseasesRisk FactorsInternal medicineMedicineAnimalsHumansPharmacology (medical)amyotrophic lateral sclerosiAmyotrophic lateral sclerosisStem cellbusiness.industryGeneral NeuroscienceMultiple sclerosistraumatic brain injuryStem-cell therapymedicine.diseasestroke030104 developmental biologyBlood-Brain Barriermultiple sclerosiParkinson’s diseaseneuroprotectionNeurology (clinical)Stem cellbusiness030217 neurology & neurosurgeryHuntington’s diseaseStem Cell TransplantationExpert review of neurotherapeutics
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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
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Lack of NG2 exacerbates neurological outcome and modulates glial responses after traumatic brain injury

2015

Traumatic brain injury (TBI) is a major cause of death and disability. The underlying pathophysiology is characterized by secondary processes including neuronal death and gliosis. To elucidate the role of the NG2 proteoglycan we investigated the response of NG2-knockout mice (NG2-KO) to TBI. Seven days after TBI behavioral analysis, brain damage volumetry and assessment of blood brain barrier integrity demonstrated an exacerbated response of NG2-KO compared to wild-type (WT) mice. Reactive astrocytes and expression of the reactive astrocyte and neurotoxicity marker Lcn2 (Lipocalin-2) were increased in the perilesional brain tissue of NG2-KO mice. In addition, microglia/macrophages with acti…

0301 basic medicinePathologymedicine.medical_specialtyMicrogliaTraumatic brain injurybusiness.industryNeurotoxicityPoison controlBrain damagemedicine.diseaseBlood–brain barrier03 medical and health sciencesCellular and Molecular Neuroscience030104 developmental biologymedicine.anatomical_structurenervous systemNeurologyGliosisImmunologymedicineNeurogliamedicine.symptombusinessGlia
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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
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