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Sida 1 från 1165 resultat
Necrosis of hippocampus and piriform lobe in 38 domestic cats with seizures: a retrospective study on clinical and pathologic findings.
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The clinical records of 38 cats (1985-1995) with a neuropathologically confirmed diagnosis of necrosis of the hippocampus and occasionally the lobus piriformis were evaluated retrospectively. There was no sex or breed predisposition. Most cats were between 1 and 6 years of age (mean age 35 months)
Feline hippocampal and piriform lobe necrosis as a consequence of severe cluster seizures in two cats in Finland.
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Feline hippocampal and piriform lobe necrosis (FHN) has been reported from several countries worldwide and is considered an important aetiology for feline epileptic seizures. The aetiology of FHN remains unclear, however it is suspected that FHN might occur secondary to intense epileptic activity as
Expression of death-associated protein kinase and recruitment to the tumor necrosis factor signaling pathway following brief seizures.
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Death-associated protein (DAP) kinase is calcium-regulated and known to function downstream of death receptors, prompting us to examine its role in the mechanism of seizure-induced neuronal death. Brief seizures were focally evoked in rats, eliciting neuronal death within the CA3 subfield of the
[Relationship between programmed cell death mechanisms and neuronal necrosis induced by seizures].
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OBJECTIVE
To clarify if programmed cell death mechanisms induced by seizures take part in the necrotic process of neurons.
METHODS
Seizure was induced by pilocarpine (P) in Sprague-Dawley adult rats which were allowed to recover for 24 or 72 hours before perfusion-fixation. Neuronal death was
Intestinal inflammation and seizure susceptibility: understanding the role of tumour necrosis factor-alpha in a rat model.
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OBJECTIVE
The aim of the study was to evaluate the correlation between colitis and susceptibility to seizures.
METHODS
Colitis was induced in Wistar rats by a single intracolonic administration of trinitrobenzene sulfonic acid (TNBS; 20 mg in 35% ethanol). The control group were given intracolonic
Caspase-3 is not activated in seizure-induced neuronal necrosis with internucleosomal DNA cleavage.
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A caspase-3-activated DNase produces internucleosomal DNA cleavage (DNA laddering). We determined whether caspase-3 is activated by lithium-pilocarpine-induced status epilepticus in six brain regions with necrosis-induced DNA laddering. The thymuses of adult rats given methamphetamine or normal
Seizure-induced neuronal necrosis: implications for programmed cell death mechanisms.
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OBJECTIVE
To determine definitively the morphology of neuronal death from lithium-pilocarpine (LPC)-and kainic acid (KA)-induced status epilepticus (SE), and to correlate this with markers of DNA fragmentation that have been associated with cellular apoptosis. Endogenous glutamate release is
Serum interleukin-1beta and tumor necrosis factor-alpha in febrile seizures: is there a link?
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OBJECTIVE
Febrile seizures are induced by fever and are the most common type of seizures in children. Although numerous studies have been performed on febrile seizures, their pathophysiology remains unclear. Recent studies have shown that cytokines may play a role in the pathogenesis of febrile
Formation of a tumour necrosis factor receptor 1 molecular scaffolding complex and activation of apoptosis signal-regulating kinase 1 during seizure-induced neuronal death.
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The consequences of activation of tumour necrosis factor receptor 1 (TNFR1) during neuronal injury remain controversial. The apoptosis signal-regulating kinase 1 (ASK1), a mitogen-activated protein kinase kinase kinase, can mediate cell death downstream of TNFR1. Presently, we examined the formation
Propionate relieves pentylenetetrazol-induced seizures, consequent mitochondrial disruption, neuron necrosis and neurological deficits in mice.
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The present research was designed to evaluate the protective effects and underlying mechanisms of propionate, a bioactive food additive, on mitochondrial disruption, neuron necrosis and neurological deficits after epilepsy seizures. Epilepsy seizures was induced by repetitive injections of
Bidirectional concentration-dependent effects of tumor necrosis factor alpha in Shigella dysenteriae-related seizures.
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We have previously demonstrated that pretreatment of mice with Shigella dysenteriae sonicate enhanced their susceptibility to pentylenetetrazole-induced seizures and that tumor necrosis factor alpha (TNF-alpha) was proconvulsive in this respect. The present study shows that TNF-alpha, at high
Interleukin-1beta, tumor necrosis factor-alpha, and nitrite levels in febrile seizures.
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Proinflammatory cytokines (such as interleukin-1beta, tumor necrosis factor-alpha) and nitric oxide are known to have both direct and indirect modulating effects on neurons and neurotoxic neurotransmitters released during excitation or inflammation. We measured interleukin-1beta, tumor necrosis
Interleukin (IL)-1beta, IL-1 receptor antagonist, IL-6, IL-8, IL-10, and tumor necrosis factor alpha gene polymorphisms in patients with febrile seizures.
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Inflammation and genetics may play a role in the pathogenesis of febrile seizures (FSs). We aimed to test whether interleukin-1beta (IL-1beta), IL-1 receptor antagonist (IL-1 Ra), IL-6 promoter, IL-8, IL-10, or tumor necrosis factor (TNF) gene polymorphisms could be used as markers of susceptibility
Molecular and functional interactions between tumor necrosis factor-alpha receptors and the glutamatergic system in the mouse hippocampus: implications for seizure susceptibility.
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Tumor necrosis factor (TNF)-alpha is a proinflammatory cytokine acting on two distinct receptor subtypes, namely p55 and p75 receptors. TNF-alpha p55 and p75 receptor knockout mice were previously shown to display a decreased or enhanced susceptibility to seizures, respectively, suggesting intrinsic
Tumor necrosis factor-alpha inhibits seizures in mice via p75 receptors.
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Brain inflammatory reactions have been described in various neurological disorders, including epilepsy. Although there is clear evidence that cytokines affect neuroglial functions and blood-brain barrier permeability, scarce information is available on the functional consequences of brain
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