oxygenase/epilepsziás roham

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Effects of hypoxia preconditioning on expression of metallothionein-1,2 and heme oxygenase-1 before and after kainic acid-induced seizures.

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Global hypoxia preconditioning provides neuroprotection against a subsequent, normally damaging challenge. While the mechanistic pathways are unknown, changes in the expression of stress-related proteins are implicated. Hypoxia preconditioning attenuates the brain edema and neuropathology associated

Febrile seizure, but not hyperthermia alone, induces the expression of heme oxygenase-1 in rat cortex.

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BACKGROUND Febrile seizure (FS) is the most common seizure disorders. Approximately one third of children with a febrile seizure have recurrent events. The mechanism of FS remains unclear. Heme oxygenase-1 (HO-1) is a member of the heat shock proteins family and can be induced in the brain by

[Effect of endogenous heme oxygenase-carbon monoxide on brain damage induced by recurrent febrile seizures].

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OBJECTIVE Febrile seizures (FS) are the most common seizure disorders in children. Approximately one third of children with a febrile seizure have recurrent events. Although most FS may not represent a serious health problem, those that are more prolonged and recurrent may cause hippocampal damage

Decreased levels of brain cyclo-oxygenase products as a possible cause of increased seizure susceptibility in convulsion-prone gerbils.

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Basal levels of 5 cerebral prostanoids (PGD2, PGF2 alpha, PGE2, 6-keto-PGF1 alpha and thromboxane/TX/B2) were measured radioimmunologically in normal and convulsion-prone gerbils. Significantly less PGD2,PGE2 and 6-keto-PGF1 alpha was found in the brain of seizure-sensitive animals. After treatment

Endogenous heme oxygenase prevents impairment of cerebral vascular functions caused by seizures.

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In newborn pigs, the mechanism of seizure-induced cerebral hyperemia involves carbon monoxide (CO), the vasodilator product of heme catabolism by heme oxygenase (HO). We hypothesized that seizures cause cerebral vascular dysfunction when HO activity is inhibited. With the use of cranial window

[Influence of nitric oxide on heme oxygenase/carbon monoxide system in hippocampus of febrile seizures rats].

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OBJECTIVE Febrile seizures (FS) are the most common type of seizure disorders. Studies have found that there have respective changes of heme oxygenase (HO)/CO system and nitric oxide synthase (NOS)/NO system during FS. The present study was to explore the influence on expression of HO-1 mRNA and

Differential expression of the astrocytic enzymes 3-hydroxyanthranilic acid oxygenase, kynurenine aminotransferase and glutamine synthetase in seizure-prone and non-epileptic mice.

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Previous investigations in seizure-prone mice have suggested that an abnormally elevated production of the astrocyte-derived neuroexcitant, quinolinic acid (QUIN), plays a role in seizure susceptibility. In order to evaluate further the role of QUIN metabolism in genetic murine seizure models, the

Antioxidant roles of heme oxygenase, carbon monoxide, and bilirubin in cerebral circulation during seizures.

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Postictal cerebrovascular dysfunction is an adverse effect of seizures in newborn piglets. The brain heme oxygenase (HO) provides protection against cerebrovascular dysfunction. We investigated the contribution of reactive oxygen species (ROS) to seizure-induced vascular damage and the mechanism of

Use of cytochrome-P450 mono-oxygenase 2 E1 isozyme inhibitors to delay seizures caused by central nervous system oxygen toxicity.

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BACKGROUND The neuronal origins and mechanisms of central nervous system oxygen toxicity are only partly understood. Oxygen free radicals are felt to play a major role in the production of CNS oxygen toxicity because of the interactions of free radicals with plasma membranes producing lipid

Heme oxygenase inhibition reduces neuronal activation evoked by bicuculline in newborn pigs.

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Carbon monoxide (CO) is a product of heme degradation by heme oxygenase (HO) that is highly expressed in the brain. The present study addresses the hypothesis that CO can be involved in brain neuronal function. The effects of the HO inhibitor, tin protoporphyrin (SnPP), on brain electrical activity

Expression of cyclo-oxygenase 2 in rat brain following kainate treatment.

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The transcriptional expression of the mitogen-inducible cyclo-oxygenase (COX-2) was investigated by in situ hybridization of kainate-treated rat brains. Kainate treatment rapidly induced COX-2 mRNA in neurons throughout the forebrain which was blocked by pretreatment with MK-801 or NBQX. Transient

Epileptic seizures increase circulating endothelial cells in peripheral blood as early indicators of cerebral vascular damage.

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Circulating endothelial cells (CECs) are nonhematopoetic mononuclear cells in peripheral blood that are dislodged from injured vessels during cardiovascular disease, systemic vascular disease, and inflammation. Their occurrence during cerebrovascular insults has not been previously described.

Carbon monoxide regulates cerebral blood flow in epileptic seizures but not in hypercapnia.

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Carbon monoxide (CO) is an endogenously produced gas sharing many properties with nitric oxide (NO), notably activating soluble guanylate cyclase and relaxing blood vessels. The brain can generate high quantities of CO from a constitutive enzyme, haem oxygenase (HO-2). To determine whether CO is

Interaction between endogenous nitric oxide and carbon monoxide in the pathogenesis of recurrent febrile seizures.

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The aim of the study was to investigate the interaction between nitric oxygenase (NOS)/nitric oxide (NO) and heme oxygenase (HO)/carbon monoxide (CO) system in the pathogenesis of recurrent febrile seizures (FS). On a rat model of recurrent FS, the ultrastructure of hippocampal neurons was observed

Differential effect of prostaglandin synthetase inhibitor pretreatment on pentylenetetrazol-induced seizures in rat.

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Release of prostaglandins (PGs) from brain tissue increases during experimentally-induced and spontaneous seizures. However, whether PGs or other arachidonic acid metabolites have a role in induction of seizures is still unclear. The effectiveness of pretreatment with PG synthetase inhibitors on

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