Search results for "general [Sun]"

showing 10 items of 3863 documents

Subchronic administration of auranofin reduced amyloid-β plaque pathology in a transgenic APPNL-G-F/NL-G-F mouse model

2020

Abstract Alzheimer’s disease (AD) is the most common cause of dementia. Neuropathological processes, including the accumulation of amyloid-β (Aβ) plaques and neurofibrillary tangles, and neuroinflammation, lead to cognitive impairment at middle and eventually later stages of AD progression. Over the last decade, focused efforts have explored repurposed drug approaches for AD pathophysiological mechanisms. Recently, auranofin, an anti-inflammatory drug, was shown to have therapeutic potential in a number of diseases in addition to rheumatoid arthritis. Surprisingly, no data regarding the effects of auranofin on cognitive deficits in AD mice or the influence of auranofin on Aβ pathology and n…

0301 basic medicinePathologymedicine.medical_specialtyAuranofinGlial fibrillary acidic proteinbiologybusiness.industryAmyloid betaGeneral NeuroscienceGlutamate decarboxylaseHippocampusPathophysiology03 medical and health sciences030104 developmental biology0302 clinical medicineSynaptic plasticitybiology.proteinMedicineNeurology (clinical)businessMolecular Biology030217 neurology & neurosurgeryNeuroinflammationDevelopmental Biologymedicine.drugBrain Research
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Autophagic vacuolar myopathy is a common feature of CLN3 disease

2018

Abstract Objective The neuronal ceroid lipofuscinoses (NCL) are genetic degenerative disorders of brain and retina. NCL with juvenile onset (JNCL) is genetically heterogeneous but most frequently caused by mutations of CLN3. Classical juvenile CLN3 includes a rare protracted form, which has previously been linked to autophagic vacuolar myopathy (AVM). Our study investigates the association of AVM with classic, non‐protracted CLN3. Methods Evaluation of skeletal muscle biopsies from three, non‐related patients with classic, non‐protracted and one patient with protracted CLN3 disease by histology, immunohistochemistry, electron microscopy, and Sanger sequencing of the coding region of the CLN…

0301 basic medicinePathologymedicine.medical_specialtyDegenerative Disordermedicine.disease_cause03 medical and health sciencessymbols.namesake0302 clinical medicineMedicineResearch ArticlesSanger sequencingMutationbusiness.industryGenetic heterogeneityGeneral NeuroscienceSkeletal muscleHistology030104 developmental biologymedicine.anatomical_structureCLN3symbolsImmunohistochemistryNeurology (clinical)business030217 neurology & neurosurgeryResearch ArticleAnnals of Clinical and Translational Neurology
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Noninvasive Monitoring of Lesion Size in a Heterologous Mouse Model of Endometriosis

2019

Here, we describe a protocol for the implementation of a heterologous mouse model in which progression of endometriosis can be assessed in real time through noninvasive monitoring of fluorescence emitted by implanted ectopic human endometrial tissue. For this purpose, biopsies of human endometrium are obtained from donor women ongoing oocyte donation. Human endometrial fragments are cultured in the presence of adenoviruses engineered to express cDNA for the reporter fluorescent protein mCherry. Upon visualization, labeled tissues with an optimal rate of fluorescence after infection are subsequently chosen for the implantation in recipient mice. One week prior to the implantation surgery, re…

0301 basic medicinePathologymedicine.medical_specialtyGeneral Chemical EngineeringEndometriosisEndometriosisHeterologousTransfectionGeneral Biochemistry Genetics and Molecular BiologyLesion03 medical and health sciencesPeritoneal cavityMice0302 clinical medicineIn vivomedicineAnimalsHumansGeneral Immunology and Microbiologybusiness.industryGeneral Neurosciencemedicine.diseaseFluorescence intensityDisease Models Animal030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisFemalemedicine.symptommCherrybusinessPreclinical imagingJournal of Visualized Experiments
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Preparation Steps for Measurement of Reactivity in Mouse Retinal Arterioles <em>Ex Vivo</em>

2018

Vascular insufficiency and alterations in normal retinal perfusion are among the major factors for the pathogenesis of various sight-threatening ocular diseases, such as diabetic retinopathy, hypertensive retinopathy, and possibly glaucoma. Therefore, retinal microvascular preparations are pivotal tools for physiological and pharmacological studies to delineate the underlying pathophysiological mechanisms and to design therapies for the diseases. Despite the wide use of mouse models in ophthalmic research, studies on retinal vascular reactivity are scarce in this species. A major reason for this discrepancy is the challenging isolation procedures owing to the small size of these retinal blo…

0301 basic medicinePathologymedicine.medical_specialtyGeneral Chemical EngineeringGlaucoma030204 cardiovascular system & hematologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineHypertensive retinopathymedicineRetinaGeneral Immunology and Microbiologybusiness.industryGeneral NeuroscienceRetinalDiabetic retinopathymedicine.disease030104 developmental biologymedicine.anatomical_structurechemistrybusinessPerfusionEx vivoBlood vesselJournal of Visualized Experiments
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Imaging in mice and men: Pathophysiological insights into multiple sclerosis from conventional and advanced MRI techniques

2019

Abstract Magnetic resonance imaging (MRI) is the most important tool for diagnosing multiple sclerosis (MS). However, MRI is still unable to precisely quantify the specific pathophysiological processes that underlie imaging findings in MS. Because autopsy and biopsy samples of MS patients are rare and biased towards a chronic burnt-out end or fulminant acute early stage, the only available methods to identify human disease pathology are to apply MRI techniques in combination with subsequent histopathological examination to small animal models of MS and to transfer these insights to MS patients. This review summarizes the existing combined imaging and histopathological studies performed in M…

0301 basic medicinePathologymedicine.medical_specialtyMultiple SclerosisNeuroimaging03 medical and health sciences0302 clinical medicineIn vivoBiopsymedicineAnimalsHumansStage (cooking)medicine.diagnostic_testbusiness.industryGeneral NeuroscienceMultiple sclerosisBrainMagnetic resonance imagingmedicine.diseaseMagnetic Resonance ImagingPathophysiology3. Good healthDisease Models AnimalEarly Diagnosis030104 developmental biologybusinessNeuroscience030217 neurology & neurosurgeryPreclinical imagingDiffusion MRIProgress in Neurobiology
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Models of cortical malformation--Chemical and physical.

2015

Abstract Pharmaco-resistant epilepsies, and also some neuropsychiatric disorders, are often associated with malformations in hippocampal and neocortical structures. The mechanisms leading to these cortical malformations causing an imbalance between the excitatory and inhibitory system are largely unknown. Animal models using chemical or physical manipulations reproduce different human pathologies by interfering with cell generation and neuronal migration. The model of in utero injection of methylazoxymethanol (MAM) acetate mimics periventricular nodular heterotopia. The freeze lesion model reproduces (poly)microgyria, focal heterotopia and schizencephaly. The in utero irradiation model caus…

0301 basic medicinePathologymedicine.medical_specialtyRodentiaHippocampal formation03 medical and health scienceschemistry.chemical_compoundGlutamatergicEpilepsy0302 clinical medicineFreezingmedicineAnimalsCerebral CortexNeocortexEpilepsybusiness.industryGeneral NeuroscienceMicrogyriaCortical dysplasiamedicine.diseaseMalformations of Cortical DevelopmentDisease Models Animal030104 developmental biologymedicine.anatomical_structureTeratogenschemistrySchizencephalybusinessNeuroscience030217 neurology & neurosurgeryIbotenic acidJournal of neuroscience methods
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Depletion of regulatory T cells increases T cell brain infiltration, reactive astrogliosis, and interferon-γ gene expression in acute experimental tr…

2019

Abstract Background Traumatic brain injury (TBI) is a major cause of death and disability. T cells were shown to infiltrate the brain during the first days after injury and to exacerbate tissue damage. The objective of this study was to investigate the hitherto unresolved role of immunosuppressive, regulatory T cells (Tregs) in experimental TBI. Methods “Depletion of regulatory T cell” (DEREG) and wild type (WT) C57Bl/6 mice, treated with diphtheria toxin (DTx) to deplete Tregs or to serve as control, were subjected to the controlled cortical impact (CCI) model of TBI. Neurological and motor deficits were examined until 5 days post-injury (dpi). At the 5 dpi endpoint, (immuno-) histological…

0301 basic medicinePathologymedicine.medical_specialtyTraumatic brain injuryRegulatory T cellT cellImmunologyT cellsExcitotoxicityBrain damagemedicine.disease_causelcsh:RC346-42903 medical and health sciencesCellular and Molecular NeuroscienceTraumatic brain injury0302 clinical medicinemedicineImmune responselcsh:Neurology. Diseases of the nervous systemInflammationGlial fibrillary acidic proteinbiologybusiness.industryResearchGeneral Neurosciencemedicine.diseaseAstrogliosisCD8A030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesbiology.proteinCytokinesMicrogliamedicine.symptombusiness030217 neurology & neurosurgeryJournal of Neuroinflammation
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Disturbed Glucose Metabolism in Rat Neurons Exposed to Cerebrospinal Fluid Obtained from Multiple Sclerosis Subjects

2017

Axonal damage is widely accepted as a major cause of permanent functional disability in Multiple Sclerosis (MS). In relapsing-remitting MS, there is a possibility of remyelination by myelin producing cells and restoration of neurological function. The purpose of this study was to delineate the pathophysiological mechanisms underpinning axonal injury through hitherto unknown factors present in cerebrospinal fluid (CSF) that may regulate axonal damage, remyelinate the axon and make functional recovery possible. We employed primary cultures of rat unmyelinated cerebellar granule neurons and treated them with CSF obtained from MS and Neuromyelitis optica (NMO) patients. We performed microarray …

0301 basic medicinePathologymedicine.medical_specialtyglucose metabolismneuromyelitis opticaBiologymultiple sclerosisArticlecerebrospinal fluidlcsh:RC321-57103 medical and health sciencesMyelin0302 clinical medicineCerebrospinal fluidDownregulation and upregulationGene expressionmedicineRemyelinationAxonlcsh:Neurosciences. Biological psychiatry. Neuropsychiatrymultiple sclerosis; glucose metabolism; neuromyelitis optica; cerebrospinal fluid; gene expressionNeuromyelitis opticaGeneral NeuroscienceMultiple sclerosismedicine.disease030104 developmental biologymedicine.anatomical_structurenervous systemgene expression030217 neurology & neurosurgery
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Mathematical model of T-cell lymphoblastic lymphoma: disease, treatment, cure or relapse of a virtual cohort of patients

2017

International audience; T lymphoblastic lymphoma (T-LBL) is a rare type of lymphoma with a good prognosis with a remission rate of 85%. Patients can be completely cured or can relapse during or after a 2-year treatment. Relapses usually occur early after the remission of the acute phase. The median time of relapse is equal to 1 year, after the occurrence of complete remission (range 0.2–5.9 years) (Uyttebroeck et al., 2008). It can be assumed that patients may be treated longer than necessary with undue toxicity. The aim of our model was to investigate whether the duration of the maintenance therapy could be reduced without increasing the risk of relapses and to determine the minimum treatm…

0301 basic medicinePediatricsmedicine.medical_specialtymedicine.medical_treatmentPopulation[SDV.CAN]Life Sciences [q-bio]/CancerPrecursor T-Cell Lymphoblastic Leukemia-LymphomachemotherapyGeneral Biochemistry Genetics and Molecular Biology[ SDV.CAN ] Life Sciences [q-bio]/Cancer03 medical and health sciences[ MATH.MATH-AP ] Mathematics [math]/Analysis of PDEs [math.AP][SDV.CAN] Life Sciences [q-bio]/CancerMaintenance therapythymusT-cell lymphoblastic lymphomamedicineHumanscancer[MATH.MATH-AP]Mathematics [math]/Analysis of PDEs [math.AP]Computer Simulationmathematical modelling[MATH.MATH-AP] Mathematics [math]/Analysis of PDEs [math.AP]educationrandomized controlled clinical trialGeneral Environmental SciencePharmacologyChemotherapyeducation.field_of_studyGeneral Immunology and Microbiologybusiness.industryApplied MathematicsGeneral NeuroscienceLymphoblastic lymphomaCancerGeneral MedicineModels Theoreticalmedicine.disease3. Good healthLymphomaSurgeryClinical trial030104 developmental biologyModeling and SimulationCohortDisease ProgressionbusinessMathematical Medicine and Biology
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(+)-Pentazocine reduces oxidative stress and apoptosis in microglia following hypoxia/reoxygenation injury

2016

Abstract Background Sigma-1 receptors (σ 1 R) are highly expressed in neurons as well as microglia and have been shown to modulate the inflammatory response in the central nervous system and thus may serve as possible target for neuroprotective strategies. The aim of the present study was to test the effect of (+)-pentazocine, a putative σ 1 R agonist, in an in vitro model of microglia activation. Methods Microglia (BV2 cells) was exposed (3 h) to 1% oxygen and reoxygenation was allowed for 24 h. Cells were treated with different concentrations (1, 10, 25 and 50 μM) of (+)-pentazocine in the presence or absence of NE-100 (1 μM), a well established σ 1 R antagonist. Cell viability and apopto…

0301 basic medicinePentazocineSigma receptorCell SurvivalmicrogliaApoptosisPharmacologyBiologymedicine.disease_causeNeuroprotection(+)-PentazocineCell LineMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePentazocine; microglia; SIGMAmedicineAnimalsReceptors sigmaViability assayAnnexin A5PhosphorylationHypoxiaMembrane Potential MitochondrialMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MicrogliaAnimalGeneral NeuroscienceApoptosiOxidative StreGlutathioneGlutathioneOxidative Stress030104 developmental biologymedicine.anatomical_structurePentazocineBiochemistrychemistryApoptosis030217 neurology & neurosurgeryIntracellularOxidative stressSIGMAmedicine.drug
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