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toluidine/epileptische aanval
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Homocysteine potentiates seizures and cell loss induced by pilocarpine treatment.
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Patients affected by recurrent seizures frequently present increased homocysteine plasma levels in consequence of treatment with antiepileptic drugs. Homocysteine is proconvulsant and can affect the response to antiepileptic drugs. In addition, high homocysteine plasma levels represent a risk factor
Neuropathological alterations in the neocortex of rats subjected to focal aminopyridine seizures.
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Acute focal seizures were produced in anaesthetized albino rats by topical application of 3- and 4-aminopyridine on the exposed fronto-parietal neocortical areas. After 15 min of seizure activity neuronal and glial changes were studied by light (toluidine blue and Golgi staining) and electron
DNA damage and nonhomologous end joining in excitotoxicity: neuroprotective role of DNA-PKcs in kainic acid-induced seizures.
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DNA repair plays a critical, but imprecisely defined role in excitotoxic injury and neuronal survival throughout adulthood. We utilized an excitotoxic injury model to compare the location and phenotype of degenerating neurons in mice (strain 129-C57BL) deficient in the catalytic subunit of the
Efficacy of melatonin on offspring liver maturation in pinealectomized pregnant rats subjected to experimental epilepsy.
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OBJECTIVE
In clinical practice, maternal epilepsy is a disabling disease for newborn infants, but current data concerning the effect of epileptic phenomena in pregnant mothers on newborns are still limited. This study was undertaken to investigate the effects of pinealectomy (Px) and melatonin
Improved selective, simple, and contrast staining of acidophilic neurons with vanadium acid fuchsin.
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Acidophilia is one of the hallmarks of acute neuronal damage and death in brain ischemia, excitotoxic and traumatic lesions and epileptic seizures. We here describe a novel and simple method for visualizing acidophilic neurons on paraffin sections, using vanadium acid fuchsin (VAF) staining and
Expression profiling reveals multiple myelin alterations in murine succinate semialdehyde dehydrogenase deficiency.
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Succinic semialdehyde dehydrogenase (SSADH) deficiency, a rare genetic defect of GABA degradation recently modelled in mice (SSADH(-/-) mice), manifests early absence seizures that evolve into generalized convulsive seizures and lethal status epilepticus in gene-ablated mice. Disrupted GABA
Leucodystrophy with pigmented glial and scavenger cells (pigmentary type of orthochromatic leucodystrophy).
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A 38-year-old man with progressive psychiatric disturbances, dysarthria, myoclonus, rigidity and terminal generalized seizures died 4 years after onset. At post-mortem, severe leucodystrophy of the centrum semi-ovale, corpus callosum and internal capsule was found. In the demyelinated areas,
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