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adenosine diphosphate/ataque epiléptico

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ArtículosEnsayos clínicosPatentes
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Acute creatine administration improves mitochondrial membrane potential and protects against pentylenetetrazol-induced seizures.

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A growing body of evidence indicates that creatine (Cr) exerts beneficial effects on a variety of pathologies where energy metabolism and oxidative stress play an etiological role. However, the benefits of Cr treatment for epileptics are still shrouded in controversy. In the present study, we found
Background: To analyze the relationship of serum ATPase activity and the levels of neuron-specific enolase (NSE), S100B protein and B-cell lymphoma/leukemia (Bcl)-2 with cognitive function in patients after epileptic seizure.

General pharmacology of the new antimuscarinic compound vamicamide.

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The general pharmacology of the new antimuscarinic compound vamicamide (FK176, (+/-)-(2R*, 4R*)-4-dimethylamino-2-phenyl-2- (2-pyridyl)valeramide, CAS 132373-81-0) was investigated using mice, rats, guinea pigs and dogs, and was in part compared with that of oxybutynin hydrochloride (oxybutynin, CAS

Coagulation abnormalities in children undergoing epilepsy surgery.

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OBJECTIVE Surgery is increasingly used to treat children with refractory epilepsy. Before surgery, the authors routinely evaluated the coagulation profile to identify coagulation abnormalities not established by personal and family history, physical examination, and routine screening

Changes in cortical and hippocampal ectonucleotidase activities in mice lacking cellular prion protein.

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Animals lacking cellular prion protein (PrP(c)) expression are more susceptible to seizures. Adenosine is an endogenous anticonvulsant agent and it levels in the synaptic cleft are regulated by ectonucleotidases. We evaluated ectonucleotidase activities in synaptosomes from hippocampus and cerebral

Pathogenesis of transient ischemic attacks and stroke in baboons.

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We describe a series of experiments in which a subhuman primate model was used to create temporary and permanent cerebral ischemia by three separate mechanisms. In the first group of five baboons, a hemodynamic model was produced by creating unilateral and bilateral carotid stenotic lesions of

Energy related metabolic alterations in diaphragm muscle resulting from acute methomyl toxicity.

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Male Sprague-Dawley rats receiving an acute dose of methomyl (5 mg/Kg, sc) developed overt signs of toxicity within 2 min. The maximum severity, including muscle fasciculations and convulsions, was attained within 7-10 min and lasted for about 30 min. A very rapid recovery followed and by 90 min

Depletion of energy metabolites following acetylcholinesterase inhibitor-induced status epilepticus: protection by antioxidants.

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Status epilepticus (SE)-induced neuronal injury may involve excitotoxicity, energy impairment and increased generation of reactive oxygen species (ROS). Potential treatment therefore should consider agents that protect mitochondrial function and ROS scavengers. In the present study, we examined

Otolaryngologic manifestations of mitochondrial cytopathies.

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BACKGROUND Primary mitochondrial cytopathies include more than 40 different identified diseases that have varied genetic features. The common factor among these diseases is that the mitochondria are unable to effectively complete oxidative phosphorylation to generate energy. One in 5000 children per

Variations of ATP and its metabolites in the hippocampus of rats subjected to pilocarpine-induced temporal lobe epilepsy.

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Although purinergic receptor activity has lately been associated with epilepsy, little is known about the exact role of purines in epileptogenesis. We have used a rat model of temporal lobe epilepsy induced by pilocarpine to study the dynamics of purine metabolism in the hippocampus during different

Metformin and trimetazidine ameliorate diabetes-induced cognitive impediment in status epileptic rats.

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Patients with diabetes and epilepsy are more prone to cognitive impairment, dementia, and even Alzheimer's disease. Diabetes-induced inflammatory process is one of the main contributing factors; however, the impact on seizure is not clear. The current study is aimed to examine the role of metformin

New mutations in TK2 gene associated with mitochondrial DNA depletion.

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Mitochondrial deoxyribonucleic acid depletion syndromes are autosomal recessive disorders characterized by a reduction of the amount of mitochondrial deoxyribonucleic acid, which impairs the synthesis of respiratory chain complexes. Mutations in the deoxyguanosine kinase and polymerase gamma genes
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