Navegando por Palavras-chave "neuronal damage"

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    C-Fos, Jun D and HSP72 immunoreactivity, and neuronal injury following lithium-pilocarpine induced status epilepticus in immature and adult rats
    (Elsevier B.V., 1998-12-10) Dube, C.; Andre, V; Covolan, Luciene [UNIFESP]; Ferrandon, A.; Marescaux, C.; Nehlig, A.; Univ Strasbourg 1; Universidade Federal de São Paulo (UNIFESP)
    In order to follow the maturation-related evolution of neuronal damage, cellular activation and stress response subsequent to Li-Pilo seizures in the 10- (P10), 21-day-old (P21) and adult rat, we analyzed the expression of the c-Fos protein as a marker of cellular activation, HSP72 immunoreactivity as the stress response and silver staining for the assessment of neuronal damage in 20 selected brain regions. the early wave of c-Fos measured at 2 h after the onset of seizures was present in most structures of the animals at the three ages studied and particularly strong in the cerebral cortex, hippocampus and amygdala. the late wave of c-Fos measured at 24 h after the onset of seizures and that was shown to correlate to neuronal damage was absent from the P10 rat brain, and present mainly in the cerebral cortex and hippocampus of P21 and adult rats. the expression of the stress response, assessed by the immunoreactivity of HSP72 at 24 h after the seizures was absent from the P10 rat brain and present in the entorhinal cortex, amygdala, hippocampus and thalamus of P21 and adult rats. the expression of Jun D at 24 h after the seizures was discrete and present in most brain regions at all ages. Neuronal injury assessed by silver staining at 6 h after the onset of seizures was very discrete in the brain of the P10 rat and limited to a few neurons in the piriform and entorhinal cortices. in older animals, marked neuronal degeneration occurred in the cerebral cortex, amygdala, hippocampus, lateral septum and thalamus. Thus the immediate cell activation induced by lithium-pilocarpine seizures which is present at all ages translates only into a late wave of c-Fos and the expression of HSP72 in P21 and adult animals in which there will be extensive cell damage. (C) 1998 Elsevier Science B.V. All rights reserved.
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    Characterization of reactive astrocytes in the chronic phase of the pilocarpine model of epilepsy
    (Blackwell Publishing Inc, 2002-01-01) Garzillo, Cibele Larrosa [UNIFESP]; Mello, Luiz Eugenio Araujo de Moraes [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Purpose: Astrogliosis is a prominent finding in human temporal lobe epilepsy. Work in animal models of temporal lobe epilepsy, however, have mostly concentrated on the acute phases of the studied models or have failed to demonstrate reactive gliosis during the chronic phases of such models.Methods: Here we used the pilocarpine model of chronic seizures and Cajal's gold sublimate technique for the staining reactive astrocytes to study this issue.Results: for half of the animals (nine of 17) subject to pilocarpine-induced status epilepticus (SE), when assessed 60 days later, variable levels of reactive astrocytes were seen in many thalamic, hippocampal, amygdalar, and neocortical areas. for the remaining half of the animals, however (eight of 17), despite a similar SE induction, as well as for controls, we could not detect stained reactive astrocytes.Conclusions: We hypothesize that these results might underlie possible differences in the frequency of recurrent spontaneous seizures.
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    Estudo dos aminoácidos neurotransmissores e da proteína Fas liquóricos nas diferentes fases da neurocisticercose humana
    (Universidade Federal de São Paulo (UNIFESP), 2010-04-28) Camargo, José Augusto [UNIFESP]; Bertolucci, Paulo Henrique Ferreira [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    The Neurocysticercosis (NCC) is the most common parasitic disease of the human central nervous system. The cysticercus may remain viable for several years, and at this stage, may modulate the inflammatory response in the host without causing symptoms. Symptoms usually appear when the cysticercus enters the stage accompanied by degenerative pericystic inflammation. These changes can lead to brain tissue and cause crisis, considered the main symptom of neurocysticercosis. Despite the economic and scientific efforts aimed at eradication and the understanding of the disease, which often affects developing countries, many questions remain little discussed. An intriguing question, and that was the central goal of this study, is the fact that some patients with NCC, which do not show signs of inflammation identified by clinical examination or imaging (CT or MRI), may or may not have seizures. The identification of markers associated with the occurrence of crises and injury could contribute to the understanding of some of these phenomeno. This study aimed to investigate in the cerebrospinal fluid of patients with neurocysticercosis, with cysts in the active phase and calcified, with no evidence of inflammation associated table and who had seizures or not, the concentration of excitatory amino acid neurotransmitters (ASPARTATE and GLUTAMATE) and inhibitory (TAURINE, glycine, glutamine and GABA mainly) and soluble Fas protein (sFAS), a marker of the extrinsic pathway of apoptosis. The control group was made up of cerebrospinal fluid from patients with disorders of the central nervous system and which were subject to minor surgeries. Fifty-eight individuals diagnosed with NCC were divided into four groups: VCWZ (active or viable cysts without seizures) n = 13; VCZ (active or viable cysts with seizures) n = 16; CCWZ (inactive or calcified cysts without seizures) n = 14; CCZ (inactive or calcified cysts with seizures) n = 15. Seventy-three subjects in the control group or without conditions were included in the study, and of these 14 were used for the quantification of SFAS and 59 for the analysis of amino acids. The groups VCWZ, VCZ, CCZ showeds a significant increase (p <5%) of SFAS when compared to the control group, suggesting the presence of apoptosis in the brain parenchyma. The significant increase in the concentration of glutamate and aspartate in the cerebrospinal fluid of patients in group VCZ reflects an increase in neuronal excitability predisposes to the occurrence of crises, despite the GABA also be increased. The increase in glutamine was detected in all groups, although it was only significant in groups with viable cysts and calcified without crises. This increase indicates that the metabolic cycle of glutamine (Gln-Glu-GABA) is increased in patients with neurocysticercosis and, when it is able to metabolize the free glutamate, concomitantly leading to the production of GABA, prevents the occurrence of crises, as observed in group CCWZ. The taurine, but increased in all groups, showed a statistical significance only in CCWZ group. Considering the results, we concluded that a disorder in the metabolism of amino acids attached the framework of neurocysticercosis, with the increase in glutamate and aspartate favoring the occurrence of crises as well as apoptosis. The changes detected in the cerebrospinal fluid of patients with calcified cysts indicate that the mechanism is also dynamic in that condition, calling the reflection of Clinical to replace the term "inactive cyst" to "reagent inactive cyst" bearing in mind that even calcified, the cyst may cause reactions in the parenchyma.
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    Long-lasting neuroprotective effect of postischemic hypothermia and treatment with an anti-inflammatory/antipyretic drug - Evidence for chronic encephalopathic processes following ischemia
    (Amer Heart Assoc, 1996-09-01) Coimbra, Cicero [UNIFESP]; Drake, M.; BorisMoller, F.; Wieloch, T.; LUND UNIV; Universidade Federal de São Paulo (UNIFESP)
    Background and Purpose It has been recognized that post ischemic pharmacological interventions may delay the evolution of neuronal damage rather than provide long-lasting neuroprotection. Also, fever complicates recovery after stroke in humans. Here we report the effects of late postischemic treatment with hypothermia and an antipyretic/anti-inflammatory drug, dipyrone, on cell damage at 1 week and 2 months of survival.Methods Rats were subjected to 10 minutes of forebrain ischemia. Hypothermia (33 degrees C) was induced at 2 hours of recovery and maintained for 7 hours. Dipyrone (100 mg . kg(-1)IP) was given every 3 hours from 14 to 72 hours of recovery. Temperature was measured every 6 hours for 60 days. Neuronal damage was assessed at 7 days and 2 months of recovery.Results From 17 to 72 hours of recovery, a period of hyperthermia was observed, which dipyrone abolished but postischemic hypothermia treatment did not. Dipyrone treatment diminished neuronal damage by 43% at 7 days, and at 2 months of survival, a minor (168) protection was seen. Postischemic hypothermia treatment alone delayed neuronal damage. In contrast, combined treatment of hypothermia followed by dipyrone markedly diminished neuronal damage by more than 50% at both 7 days and 2 months of recovery.Conclusions Neuronal degeneration may be ongoing for months after a transient ischemic insult, and prolonged protective measures need to be instituted for long-lasting neuroprotective effects. Hyperthermia during recovery worsens ischemic damage, and processes associated with inflammation may contribute to the development of neuronal damage. An early and extended period of postischemic hypothermia provides a powerful and long-lasting protection if followed by treatment with anti-inflammatory/antipyretic drugs.
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    Quantification of Fas protein in CSF of patients with neurocysticercosis
    (Academia Brasileira de Neurologia - ABNEURO, 2012-04-01) Camargo, José Augusto [UNIFESP]; Bertolucci, Paulo Henrique Ferreira [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Neurocysticercosis is a parasitic disease that affects the central nervous system. The objective of this study was to investigate the correlation between neuronal death evaluated by the quantification of Fas apoptotic factor and the different evolutive forms of neurocysticercosis accompanied or not by epileptic seizures. METHODS: Cerebrospinal fluid samples from 36 patients with a diagnosis of neurocysticercosis divided into the following groups: active cystic form (n=15), 9 patients with and 6 without seizures, and calcified form (=21), 9 with and 12 without seizures. Fourteen patients comprised the control group. Fas protein concentrations were determined by ELISA. RESULTS: Only the group of patients with calcified cysts without seizures presented cerebrospinal fluid levels of Fas similar to those of the control group. Higher levels were observed for the other groups. CONCLUSIONS: The present finding suggests high cerebrospinal fluid levels of soluble Fas protein, except for patients with calcified cysts without seizures. Significant differences were observed for the group with calcified cysts and seizures, suggesting greater neuronal damage in these patients. Replacement of the term inactive cyst with reactive inactive cyst is suggested.