acetone/seizures

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Evaluation of the anticonvulsant activity of the seed acetone extract of Ferula gummosa Boiss. against seizures induced by pentylenetetrazole and electroconvulsive shock in mice.

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Ingia / Ingia

Ferula gummosa Boiss. (Apiaceae) which has been used as an antiepileptic remedy in Iranian traditional medicine was evaluated for anticonvulsant activity against experimental seizures. The seed acetone extract of F. gummosa protected mice against tonic convulsions induced by maximal electroshock

Ketogenic diet: does acetone stop seizures?

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Ingia / Ingia

BACKGROUND The mechanism of action of the ketogenic diet, a therapy for refractory epilepsy, is unknown. Our hypothesis is that acetone, one of three ketones elevated by the ketogenic diet, is directly responsible for the diet's anticonvulsant effects. This study examined the basic concepts of this

Possible mechanism for the effect of ketogenic diet in cases of uncontrolled seizures. The reconsideration of acetone theory.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

High fat and low carbohydrate diet, designated ketogenic diet, has been successfully used for the treatment of intractable epilepsy in a portion of patients, particularly in children. Several hypotheses have been worked out for the explanation of its beneficial effects, among others acetone has been

[Effect of acetone upon pentamethylenetetrazole convulsions].

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Ingia / Ingia

Immunohistochemical localization of P-glycoprotein in rat brain and detection of its increased expression by seizures are sensitive to fixation and staining variables.

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Ingia / Ingia

The MDR1 gene product, P-glycoprotein (P-gp), was shown to confer multidrug resistance to cancer cells, but its overexpression is also suggested to be involved in pharmacoresistance of epilepsy by acting as an energy-dependent drug-efflux pump in the blood-brain barrier (BBB). In normal brain

Acetone potentiation of acute acetonitrile toxicity in rats.

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Ingia / Ingia

The purpose of these studies was to investigate the nature and mechanism of a toxicologic interaction between acetonitrile and acetone. Results of oral dose-response studies utilizing a 1:1 (w/w) mixture of acetonitrile and acetone, or varying doses of acetonitrile administered together with a

Pattern of inhalation exposure: blood levels and acute subnarcotic effects of toluene and acetone in rats.

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Ingia / Ingia

Solvent blood concentrations and subnarcotic effects (inhibition of electrically evoked seizures) were measured in rats exposed to constant or fluctuating air concentrations of toluene or acetone. A 4 hour exposure of resting rats to toluene at an air concentration of 1 and 2 mg/l, or to acetone at

Anticonvulsant activity of DNS II fraction in the acute seizure models.

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Ingia / Ingia

OBJECTIVE Delphinium nordhagenii belongs to family Ranunculaceae, it is widely found in tropical areas of Pakistan. Other species of Delphinium are reported as anticonvulsant and are traditionally used in the treatment of epilepsy. Delphinium nordhagenii is used by local healer in Pakistan but never

The anticonvulsant activity of acetone, the major ketone body in the ketogenic diet, is not dependent on its metabolites acetol, 1,2-propanediol, methylglyoxal, or pyruvic acid.

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Ingia / Ingia

BACKGROUND Acetone, one of the principal ketone bodies elevated during treatment with the ketogenic diet, exhibits anticonvulsant properties that may contribute to the seizure protection conferred by the diet. The anticonvulsant mechanism of acetone is unknown, but it is metabolized to several

Anticonvulsant effects of methyl ethyl ketone and diethyl ketone in several types of mouse seizure models.

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Ingia / Ingia

The anticonvulsant effects of acetone have been reported in various animal models of epilepsy. We recently demonstrated that other ketone bodies, methyl ethyl ketone (MEK) and diethyl ketone (DEK), suppressed status epilepticus that was induced by lithium-pilocarpine in rat. In the present study,

Pharmacodynamic and pharmacokinetic interactions between common antiepileptic drugs and acetone, the chief anticonvulsant ketone body elevated in the ketogenic diet in mice.

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Ingia / Ingia

OBJECTIVE Acetone is the principal ketone body elevated in the ketogenic diet (KD), with demonstrated robust anticonvulsant properties across a variety of seizure tests and models of epilepsy. Because the majority of patients continue to receive antiepileptic drugs (AEDs) during KD treatment,

Acetoacetate, acetone, and dibenzylamine (a contaminant in l-(+)-beta-hydroxybutyrate) exhibit direct anticonvulsant actions in vivo.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

OBJECTIVE To investigate whether ketone bodies are directly anticonvulsant. METHODS We tested the effects of acetoacetate (ACA), acetone, and both stereoisomers, D-(-)- and L-(+), of beta-hydroxybutyrate (BHB) on sensory-evoked seizures in Frings audiogenic seizure-susceptible mice. RESULTS We found

Acetone as an anticonvulsant.

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Ingia / Ingia

Recent interest in the anticonvulsant effects of acetone has stemmed from studies related to the ketogenic diet (KD). The KD, a high-fat diet used to treat drug-resistant seizures, raises blood and brain levels of three ketones: beta-hydroxybutyrate, acetoacetate, and acetone. An obvious question is

Neutrotropic effects and blood levels of solvents at combined exposures: binary mixtures of toluene, o-xylene and acetone in rats and mice.

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Ingia / Ingia

Male rats and female mice were exposed to vapours of toluene, o-xylene and acetone in basic or double concentrations or to binary combinations of basic concentrations, for 4 and 2 hours, respectively. Basic air concentrations were for rats and mice (in ppm): toluene 270 and 380, o-xylene 230 and

Convulsive seizure induced by intracerebral injection of semicarbazide (an anti-vitamin B6) in the mouse.

Watumiaji waliosajiliwa tu ndio wanaweza kutafsiri nakala

Ingia / Ingia

The direct injection of semicarbazide (SC), an antivitamin B6 (anti-B6), into the lateral ventricle of the mouse brain induced convulsion and tremors at a smaller dose after a shorter latent period than that in systemic administration. The symptoms were prevented by pyridoxine, aminooxyacetic acid

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