citrulline/эпилептический припадок

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Evidence for the involvement of L-citrulline but not nitric oxide in the proconvulsant action of the precursor L-arginine on picrotoxin-induced convulsions in rats.

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To determine the role of the metabolites of L-arginine in its actions on picrotoxin-induced convulsions in rats, the concentrations of nitric oxide (NO) and L-citrulline were measured in the brain 30 and 60 min after the administration of L-arginine (1000 and 2000 mg/kg) or of N-nitro-L-arginine

A patient with type II citrullinemia who developed refractory complex seizure.

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A 31-year-old Japanese male was admitted to our hospital for refractory complex seizures. He had no history on medical or psychiatric illness. He began to exhibit aberrant behavior accompanied by cloudiness of consciousness. Thereafter, he exhibited partial seizures followed by a twilight state or

Accumulation of cytotoxins during the development of seizures and edema after hypoxic-ischemic injury in late gestation fetal sheep.

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Several hours after an hypoxic-ischemic injury to the developing brain, hyperemia, then seizures, edema, and infarction can develop. The roles of nitric oxide (NO) synthesis and excitotoxin accumulation during these later phases of injury are not known. The time course of extracellular levels of

Anticonvulsant effects of 7-nitroindazole in rodents with reflex epilepsy may result from L-arginine accumulation or a reduction in nitric oxide or L-citrulline formation.

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1. To investigate the role of nitric oxide in epilepsy we have studied the effects of agents which affect nitric oxide synthesis in sound-induced seizures in DBA/2 mice and in genetically epilepsy-prone (GEP) rats. 2. The neuronal selective nitric oxide synthase inhibitor, 7-nitroindazole (7-NI) is

Systemic administration of lithium chloride and tacrine but not kainic acid augments citrulline content of rat brain.

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The effects of tacrine (5 mg/kg i.p.) in lithium chloride (LiCl; 12 mEq/kg i.p.)-pretreated (24 h beforehand) animals and of kainate (10 mg/kg i.p.) on brain citrulline, the co-product of nitric oxide (NO) synthesis, were studied in rats. High performance liquid chromatography analysis of whole

Stroke-like episodes, peri-episodic seizures, and MELAS mutations.

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OBJECTIVE Stroke-like episodes (SLEs) are a hallmark of various mitochondrial disorders, in particular MELAS syndrome. SLEs manifest with vasogenic oedema (DWI and ADC hyperintensity) or partial cytotoxic oedema (DWI hyperintensity, ADC hypointensity) in the acute and subacute stage, and with

Delta1-pyrroline-5-carboxylate synthase deficiency: neurodegeneration, cataracts and connective tissue manifestations combined with hyperammonaemia and reduced ornithine, citrulline, arginine and proline.

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Delta1-pyrroline-5-carboxylate synthase (P5CS) catalyses the reduction of glutamate to Delta1-pyrroline-5-carboxylate, a critical step in the biosynthesis of proline, ornithine and arginine. Recently, we reported a newly recognised inborn error due to deficiency of P5CS in two sibs, one presenting

Citrulline and ammonia accumulating in citrullinemia reduces antioxidant capacity of rat brain in vitro.

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Citrullinemia is an inborn error of the urea cycle caused by deficient argininosuccinate synthetase, which leads to accumulation of L-citrulline and ammonia in tissues and body fluids. The main symptoms include convulsions, tremor, seizures, coma, and brain edema. The pathophysiology of the

Brain amino acid levels are related to seizure propensity in the gerbil (Meriones unguiculatus).

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1. Gerbils were scored for seizure severity and duration and ambulatory and rearing behaviours on presentation with an "open field". 2. Eight seizure-prone (SP) and eight non-seizure-prone (NSP) gerbils were killed and their brains treated to inactivate enzymes before division into corticate and

Prevention of kainic acid seizures-induced changes in levels of nitric oxide and high-energy phosphates by 7-nitroindazole in rat brain regions.

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Previous studies using the spin trapping agent N-tert-butyl-alpha-phenylnitrone (PBN) and the antioxidant vitamin E established the involvement of free radicals in kainic acid (KA)-induced neurotoxicity. In the present study, we examined the effects of the neuronal nitric oxide synthase (nNOS)

CE-MS metabolic profiling of volume-restricted plasma samples from an acute mouse model for epileptic seizures to discover potentially involved metabolomic features

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Currently, a high variety of analytical techniques to perform metabolomics is available. One of these techniques is capillary electrophoresis coupled to mass spectrometry (CE-MS), which has emerged as a rather strong analytical technique for profiling polar and charged compounds. This work aims to

[Clinical characteristics and analysis of mass spectrometric data in patients with ornithine transcarbamylase deficiency].

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OBJECTIVE To explore the clinical manifestations and biochemical characteristics of patients with ornithine transcarbamylase deficiency (OTCD) so as to increase the clinician awareness for this disease. METHODS The clinical manifestations, blood ammonia levels, citrulline levels, urinary orotic acid

[Analysis of clinical features, metabolic profiling and gene mutations of patients with ornithine transcarbamylase deficiency].

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OBJECTIVE To analyze the clinical features, metabolic profiling and gene mutations of patients with ornithine transcarbamylase deficiency (OTCD) and explore the molecular pathogenesis of OTCD in order to provide a solution for molecular diagnostics and genetic counseling. METHODS Clinical data of 3

[Chronic hyperammonemia with orotic aciduria: evidence of pyrimidine pathway stimulation (author's transl)].

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We have investigated a 3 year old girl with mental and physical retardation, chronic hyperammonemia and orotic aciduria. Plsma glutamine, alanine and proline concentrations were high. Alanine was present in her urine. She excreted only half the urea of control subjects on a similar protein intake.

Down-Regulation of Porcine Heart Diaphorase Reactivity by Trimanganese Hexakis(3,5-Diisopropylsalicylate), Mn(3)(3,5-DIPS)6, and Down-Regulation of Nitric Oxide Synthase Reactivity by Mn(3)(3,5-DIPS)(6) and Cu(II)(2)(3,5-DIPS)(4).

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Purposes of this work were to examine the plausible down-regulation of porcine heart diaphorase (PHD) enzyme reactivity and nitric oxide synthase (NOS) enzyme reactivity by trimanganese hexakis(3,5-diisopropylsalicylate), [Mn(3)(3,5-DIPS)(6)] as well as dicopper tetrakis(3,5- diisopropylsalicylate,

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