Search results for "NERVE"

showing 10 items of 1683 documents

The Neuroepithelium Disruption Could Generate Autoantibodies against AQP4 and Cause Neuromyelitis Optica and Hydrocephalus

2014

Neuromyelitis optica is an inflammatory disease characterized by neuritis and myelitis of the optic nerve. Its physiopathology is connected with the aquaporin-4 water channel, since antibodies against aquaporin-4 have been found in the cerebrospinal fluid and blood of neuromyelitis optica patients. The seropositivity for aquaporin-4 antibodies is used for the diagnosis of neuromyelitis optica or neuromyelitis optica spectrum disease. On the other hand, aquaporin-4 is expressed in astrocyte feet in the brain-blood barrier and subventricular zones of the brain ventricles. Aquaporin-4 expression is high in cerebrospinal fluid in hydrocephalus. Furthermore, neuroepithelial denudation precedes n…

Pathologymedicine.medical_specialtyNeuromyelitis opticabusiness.industryurogenital systemNeuritisMyelitisReview Articlemedicine.diseasePathophysiologyeye diseasesHydrocephalusNeuroepithelial cellCerebrospinal fluidmedicineOptic nervebusinessInternational Scholarly Research Notices
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Reactive neurogenesis during regeneration of the lesioned medial cerebral cortex of lizards

1995

Abstract This study reports that lesion of the adult lizard medial cortex (lizard hipocampal fascia dentata) induces a short period of intensive neurogenesis which we have termed reactive neurogenesis; a cell proliferation event that occurs in the subjacent ependyma. Specific lesion of the medial cortex was achieved by intraperitoneal injection of the neurotoxin 3-acetylpyridine and proliferating cells were detected using tritiated thymidine or 5-bromodeoxiuridine pulse labelling. After lesion, granule neurons in the lizard medial cortex cell layer appeared pyknotic and died; they were then removed and progressively replaced by a set of new neurons. These neurons were mostly generated from …

Pathologymedicine.medical_specialtyPyridinesMedial cortexNeurotoxinsPodarcis hispanicaLesionNeuroblastmedicineAnimalsCerebral CortexbiologyGeneral NeuroscienceNeurogenesisLizardsDNAAnatomybiology.organism_classificationImmunohistochemistryNerve RegenerationMicroscopy Electronmedicine.anatomical_structureCerebral cortexAutoradiographyFascia dentatamedicine.symptomEpendymaCell DivisionNeuroscience
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Transitory disappearance of microglia during the regeneration of the lizard medial cortex

1994

In normal lizards, microglial cells populate the medial cortex (a zone homologous to the hippocampal fascia dentata), with a preferential distribution along the border between the granular cell layer and the plexiform layers. Intraperitoneal injection of the neurotoxin 3-acetylpyridine (3AP) induces a selective lesion in the medial cortex with a rapid degeneration of the granular layer and its zinc-enriched axonal projection. Within 6-8 weeks, the granular layer is, however, re- populated by a new set of neurons generated in the subjacent ependyma and the cell debris is removed. The aim of this study was to determine to what extent microglia were involved in the scavenging processes during …

Pathologymedicine.medical_specialtyPyridinesMedial cortexPopulationHippocampusGranular layerHippocampal formationBiologyHippocampusCellular and Molecular NeurosciencePhagocytosisCortex (anatomy)medicineAnimalseducationeducation.field_of_studyHistocytochemistryLizardsAnatomyAcid Anhydride HydrolasesNerve RegenerationMicroscopy Electronmedicine.anatomical_structureNeurologyNeurogliaFascia dentataMicrogliaGlia
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BDNF, but not NT-4, is necessary for normal development of Meissner corpuscles.

2005

Abstract Meissner corpuscles are rapidly adapting cutaneous mechanoreceptors depending for development on TrkB expressing sensory neurons, but it remains to be established which of the known TrkB ligands, BDNF or NT-4, is responsible of this dependence. In this study we analyze Meissner corpuscles in the digital pads of mice with target mutations in the genes encoding for either BDNF or NT-4, using immunohistochemistry and transmission-electron microscopy, and they were identified based on their morphology and expression of S100 protein. All wild-type animals as well as NT-4 −/− animals and BDNF and NT4 heterozygous animals have Meissner corpuscles that are normal in number and size. Howeve…

Pathologymedicine.medical_specialtyRatónTropomyosin receptor kinase BLigandsS100 proteinMicemedicineAnimalsReceptor trkBNerve Growth FactorsBrain-derived neurotrophic factorMice KnockoutbiologyChemistryGeneral NeuroscienceBrain-Derived Neurotrophic FactorCell biologyMechanoreceptorMice Inbred C57BLmedicine.anatomical_structurenervous systemMeissner Corpusclebiology.proteinImmunohistochemistryMechanoreceptorsNeurotrophinNeuroscience letters
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S100α and S100β proteins in human cutaneous sensory corpuscles: Effects of nerve and spinal cord injury

1998

S100 protein in the vertebrate peripheral nervous system consists of homo- or heterodimers of S100α and S100β proteins, the first predominating in neurons and the second in glial cells. Recently, however, occurrence of S100β protein in neurons has been reported. The expression of S100 protein by Schwann cells, as well as their derivatives in sensory corpuscles, depends on the sensory axon (i.e., the Schwann cell–axon contact). The present study analyzed the distribution of S100α and S100β proteins in human cutaneous sensory corpuscles and the effects of peripheral or central sensory axon severance in the expression of these proteins. Simple or double immunohistochemistry was carried out usi…

Pathologymedicine.medical_specialtySensory systemBiologyConfocal scanning microscopyNerve injurymedicine.diseaseAgricultural and Biological Sciences (miscellaneous)S100 proteinmedicine.anatomical_structurePeripheral nervous systemmedicineAnatomyAxonmedicine.symptomSpinal cord injuryImmunostainingThe Anatomical Record
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AN ULTRASTRUCTURAL STUDY OF THE RETINA IN HUMAN LATE INFANTILE NEUROAXONAL DYSTROPHY

1993

A case involving a girl who died at 11 years of age and who had developed normally until the age of 18 months, at which time further psychomotor maturation stopped and then regressed, is reported. The patient appeared hypotonic and showed loss of deep tendon reflexes, as well as bulbar signs and increasing immobility. Visual impairment resulted in blindness at the age of 7 years. Her disease was diagnosed as late infantile neuroaxonal dystrophy (LINAD) after examination of sural nerve biopsy samples and after autopsy. Under electron microscopy, retinal axons were filled with tubulocisternal profiles and occasional large lamellar clefts close to or distant from synaptic complexes. These lesi…

Pathologymedicine.medical_specialtySural nerveAutopsyRetinaInfantile neuroaxonal dystrophychemistry.chemical_compoundRetinal DiseasesSural NerveHumansMedicineChildOuter nuclear layerMedulla OblongataRetinabusiness.industryMusclesRetinalHypertrophyGeneral Medicinemedicine.diseaseAxonsOphthalmologymedicine.anatomical_structurechemistryNerve DegenerationUltrastructureMedulla oblongataFemaleNervous System DiseasesbusinessRetina
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Clinical spectrum of BICD2 mutations.

2020

Background and purpose Mutations in the BICD2 gene cause autosomal dominant lower extremity-predominant spinal muscular atrophy 2A (SMALED2A), a condition that is associated with a specific pattern of thigh and calf muscle involvement when studied by magnetic resonance imaging (MRI). Patients may present minor clinical sensory impairment, but objective sensory involvement has yet to be demonstrated. Methods We collected clinical data from 11 patients from five different families carrying mutations in BICD2. Genetic diagnosis was achieved using gene panel testing and skin biopsies were taken from two patients to study the epidermal nerve fiber density. Results In the studied patients, three …

Pathologymedicine.medical_specialtyWeaknessSensory systemNerve fiberBICD2 Charcot-Marie-Tooth hereditary motor neuropathy muscle magnetic resonance imaging spinal muscular atrophyThighmedicine.disease_causeMuscular Atrophy Spinal03 medical and health sciences0302 clinical medicineCharcot-Marie-Tooth DiseasemedicineHumans030212 general & internal medicineMuscle SkeletalMutationLegmedicine.diagnostic_testbiologybusiness.industryMagnetic resonance imagingSpinal muscular atrophymedicine.diseasebiology.organism_classificationMagnetic Resonance ImagingMediusmedicine.anatomical_structureNeurologyMutationNeurology (clinical)medicine.symptombusinessMicrotubule-Associated Proteins030217 neurology & neurosurgery
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Improved Regeneration of Autologous Nerve Transplants by Means of VEGF-Gene Therapy

2009

The impact of the Vascular Endothelial Growth Factor (VEGF) on the angiogenic cascade is proven. Recently its neuroprotective effect after peripheral nerve injuries on α-motoneurons in the spinal cord was shown. Experiments on α-motoneurons demonstrated a decreased sensitivity to ischemia under VEGF-therapy. Aim of the study was to elucidate the effect of a localized VEGF-gene-therapy using an adenoviral vector construct in the model of a peripheral nerve defect in the rat treated with an autologous nerve transplant.

Pathologymedicine.medical_specialtybiologybusiness.industryVEGF receptorsIschemiaSpinal cordmedicine.diseaseNeuroprotectionViral vectorVascular endothelial growth factorchemistry.chemical_compoundmedicine.anatomical_structurechemistryPeripheral nerveDecreased Sensitivitybiology.proteinMedicinebusiness
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Chapter 35 Transcranial magnetic stimulation in brainstem lesions and lesions of the cranial nerves

2003

Publisher Summary This chapter focuses on transcranial magnetic stimulation (TMS) applications in brainstem pathology and on the description of TMS techniques for the evaluation of motor cranial nerve function, which is an essential measure in the diagnostic workup of brain-stern lesions. Applications of TMS to the cranial nerve innervated muscles have been the objective of numerous investigations, ranging from basic neuroanatomic studies to determine the central course of corticonuclear projections to clinical applications carried out to determine the location of lesions, investigate the pathophysiology of ischemic dysarthria, detect clinically silent lesions in multiple sclerosis, obtain …

Pathologymedicine.medical_specialtybusiness.industrymedicine.medical_treatmentCranial nervesAnatomyMotor neuronmedicine.diseaseFacial nerveFacial paralysisTranscranial magnetic stimulationDysarthriamedicine.anatomical_structureCranial Nerve InjuryHypoglossal Nerve Diseasesmedicinemedicine.symptombusiness
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Malignant peripheral nerve sheath tumor of the maxila

2005

Summary We present a case of a malignant peripheral nerve sheath tumor [MPNST] of the maxilla corresponding to a 12 year old male who had a painful, ulcerated rapid growing tumor. Histology revealed the presence of a tumor consisting of fusiform cells with abundant mitosis, with negative cytokeratins, actin, desmin, myoglobin and factor VIII. In contrast, the protein S-100 was positive. MPNST was not associated with signs of Neurofibromatosis Type 1. The patient was surgically intervened and received radiotherapy, then died within 10 months posterior to surgical intervention after suffering recurrence.

Pathologymedicine.medical_specialtybusiness.industrymedicine.medical_treatmentHistologyMalignant peripheral nerve sheath tumormedicine.diseasePathology and Forensic MedicineRadiation therapyNeurosarcomaOncologyOtorhinolaryngologyMaxillaMaxillaMedicineDesminMalignant peripheral nerve sheath tumorNeurofibromatosisOral SurgerybusinessOral Oncology Extra
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