Remyelination
Mostrando 1-12 de 39 artigos, teses e dissertações.
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1. Propentofylline reverses delayed remyelination in streptozotocin-induced diabetic rats
Objective The diabetic state induced by streptozotocin injection is known to impair oligodendroglial remyelination in the rat brainstem following intracisternal injection with the gliotoxic agent ethidium bromide (EB). In such experimental model, propentofylline (PPF) recently showed to improve myelin repair, probably due to its neuroprotective, antiinflamm
Arch. Endocrinol. Metab.. Publicado em: 2015-02
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2. O MODELO DESMIELINIZANTE DO BROMETO DE ETÍDIO (BE): ESTUDOS MORFOLÓGICOS EM CAMUNDONGOS C57BL/6 NORMAIS E KNOCKOUT PARA CONEXINA 32 / ETHIDIUM BROMIDE (EB) DEMYELINATING MODEL: MORPHOLOGIC STUDIES IN C57BL/6 NORMAL AND CX 32 KNOCKOUT MICE
Light and ultraestructural changes of central and peripheral nervous system lesions in mice KO for connexin-32 and submitted to the ethidium bromide gliotoxic demyelinating model are described. Their KO condition was tested with PCR and a negative connexin-32 labelling was performed by immunofluorescence. The experimental animals were C57BL/6 normal mice and
Publicado em: 2007
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3. Delayed Schwann cell and oligodendrocyte remyelination after ethidium bromide injection in the brainstem of Wistar rats submitted to streptozotocin diabetogenic treatment
Schwann cell disturbance followed by segmental demyelination in the peripheral nervous system occurs in diabetic patients. Since Schwann cell and oligodendrocyte remyelination in the central nervous system is a well-known event in the ethidium bromide (EB) demyelinating model, the aim of this investigation was to determine the behavior of both cell types aft
Brazilian Journal of Medical and Biological Research. Publicado em: 2006-05
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4. ASTROCYTIC AND OLIGODENDROGLIAL RESPONSE OF THE BRAIN STEM OF IMMUNOSUPPRESSED WISTAR RATS SUBMITTED TO THE ETHIDIUM BROMIDE DEMYELINATING MODEL / RESPOSTA ASTROCITÁRIA E OLIGODENDROGLIAL NO TRONCO ENCEFÁLICO DE RATOS WISTAR IMUNOSSUPRIMIDOS E SUBMETIDOS AO MODELO DESMIELINIZANTE DO BROMETO DE ETÍDIO
Remielinização após desmielinização com brometo de etídio (BE) no tronco encefálico de ratos é realizada por oligodendrócitos e células de Schwann que invadem o tecido após a morte dos astrócitos. Embora a remielinização por oligodendrócitos seja detectada a partir dos 13 dias pós-intoxicação, a origem das células remielinizantes não é c
Publicado em: 2005
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5. Ethidium bromide-induced demyelination of the sciatic nerve of adult Wistar rats
Peripheral nerve ultrastructure was assessed after single or multiple local injections of the intercalating dye ethidium bromide. Thirty-four adult Wistar rats of both sexes were divided into five groups and maintained in a controlled environment with rat chow and water ad libitum throughout the experiment. The experimental animals were injected with 1 µl o
Brazilian Journal of Medical and Biological Research. Publicado em: 2002-01
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6. The extracellular matrix in multiple sclerosis: an update
Extracellular matrix (ECM) molecules play important roles in the pathobiology of the major human central nervous system (CNS) inflammatory/demyelinating disease multiple sclerosis (MS). This mini-review highlights some recent work on CNS endothelial cell interactions with vascular basement membrane ECM as part of the cellular immune response, and roles for w
Brazilian Journal of Medical and Biological Research. Publicado em: 2001-05
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7. Promotion of remyelination by polyclonal immunoglobulin in Theiler's virus-induced demyelination and in multiple sclerosis.
Spontaneous remyelination occurs in experimental models of demyelination and in patients with multiple sclerosis, although to a limited extent. This enables the search for factors that promote remyelination. Using the Theiler's virus model of central nervous system demyelination, promotion of remyelination was observed after passive transfer of CNS-specific
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8. Human monoclonal antibodies reactive to oligodendrocytes promote remyelination in a model of multiple sclerosis
Promoting remyelination, a major goal of an effective treatment for demyelinating diseases, has the potential to protect vulnerable axons, increase conduction velocity, and improve neurologic deficits. Strategies to promote remyelination have focused on transplanting oligodendrocytes (OLs) or recruiting endogenous myelinating cells with trophic factors. Ig-b
National Academy of Sciences.
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9. Sequence of demyelination-remyelination in Guillain-Barré disease.
A detailed investigation of nerve conduction was made in a patient with Guillain-Barré disease. Conduction velocity and configuration of the compound action potential in distal (median), intermediate (tibial) and central (sciatic) nerve segments were studied serially as the patient weakened and then recovered. Demyelination was found to follow a centripetal
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10. Thyroid hormone administration enhances remyelination in chronic demyelinating inflammatory disease
Chronic disabilities in multiple sclerosis are believed to be due to neuron damage and degeneration, which follow remyelination failure. Due to the presence of numerous oligodendrocyte precursors inside demyelination plaques, one reason for demyelination failure could be the inability of oligodendrocyte precursor cells to turn into myelinating oligodendrocyt
National Academy of Sciences.
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11. Notch1 signaling plays a role in regulating precursor differentiation during CNS remyelination
In the developing CNS, Notch1 and its ligand, Jagged1, regulate oligodendrocyte differentiation and myelin formation, but their role in repair of demyelinating lesions in diseases such as multiple sclerosis remains unresolved. To address this question, we generated a mouse model in which we targeted Notch1 inactivation to oligodendrocyte progenitor cells (OP
National Academy of Sciences.
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12. Growth changes in sensory nerve fibre aggregates undergoing remyelination