glucose 6 phosphate dehydrogenase/seizures

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The New CIC Mutation Associates with Mental Retardation and Severity of Seizure in Turkish Child with a Rare Class I Glucose-6-Phosphate Dehydrogenase Deficiency

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Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked recessive disease that causes acute or chronic hemolytic anemia and potentially leads to severe jaundice in response to oxidative agents. Capicua transcriptional repressor (CIC) is an important gene associated with mental

Glucose-6-phosphate dehydrogenase deficiency presented with convulsion: a rare case.

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Red blood cells carry oxygen in the body and Glucose-6-Phosphate Dehydrogenase protects these cells from oxidative chemicals. If there is a lack of Glucose-6-Phosphate Dehydrogenase, red blood cells can go acute hemolysis. Convulsion is a rare presentation for acute hemolysis due to

Anemia, cataracts, and seizures in patient with glucose-6-phosphate dehydrogenase deficiency.

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Acute rhabdomyolysis induced by tonic-clonic epileptic seizures in a patient with glucose-6-phosphate dehydrogenase deficiency.

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The genetic risk of acute seizures in African children with falciparum malaria.

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OBJECTIVE It is unclear why some children with falciparum malaria develop acute seizures and what determines the phenotype of seizures. We sought to determine if polymorphisms of malaria candidate genes are associated with acute seizures. METHODS Logistic regression was used to investigate genetic

Evaluation of glutathione metabolism in NMDA preconditioning against quinolinic acid-induced seizures in mice cerebral cortex and hippocampus.

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Brain preconditioning refers to a wide range of treatments that induce a neuronal tolerance state where neuronal tissue become more resistant to a subsequent lethal insult. The mechanisms underlying the preconditioning-induced brain tolerance are not fully understood, but up-regulation of

Is glucose-6-phosphate dehydrogenase deficiency a risk factor for hyperbaric oxygen exposure?

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Divers and patients lacking glucose-6-phosphate dehydrogenase (G6PD) may face a serious threat of central nervous system oxygen toxicity (CNS-OT) during exposure to hyperbaric oxygen (HBO), due to the important part played by G6PD in cellular redox balance. Our objective was to investigate G6PD

Cerebral oxidized and reduced nicotinamide-adenine dinucleotide phosphate and glucose 6-phosphate dehydrogenase in mice during exposure to high oxygen pressure.

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NADP+, NADPH and glucose 6-phosphate dehydrogenase were determined in the cerebral cortex of mice exposed to high O2 pressure for 0, 8 and 16 min. These time intervals corresponded to 0, 50 and 100% of the CT50 (the time taken for 50% of the mice to convulse). Cerebral NADP+, NADPH and glucose

Severe malaria and glucose-6-phosphate-dehydrogenase deficiency: a reappraisal of the malaria/G-6-P.D. hypothesis.

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Nigerian children with convulsions and Plasmodium falciparium parasitaemia above 100,000/microliter did not show a decreased frequency of glucose-6-phosphate-dehydrogenase (G.-6-P.D.) deficiency. A re-evaluation of earlier studies has led to the conclusion that clinical evidence of protection

Effect of pentylenetetrazol-induced epileptic seizure on the antioxidant enzyme activities, glutathione and lipid peroxidation levels in rat erythrocytes and liver tissues.

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OBJECTIVE In order to clarify whether oxidative stress accompanies epilepsy, we examined the effects of pentylenetetrazol (PTZ)-induced epilepsy on the lipid peroxidation and antioxidant enzyme activities in erythrocytes and liver tissues of adult Wistar rats. METHODS The activities of antioxidative

Hemolysis and methemoglobinemia secondary to rasburicase administration.

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OBJECTIVE To report a case of hemolytic anemia and methemoglobinemia developing after rasburicase administration to a patient with glucose-6-phosphate dehydrogenase (G6PD) deficiency. METHODS A 50-year-old African American man was hospitalized with new onset seizure, diabetic ketoacidosis,

Intracerebroventricular administration of N-acetylaspartic acid impairs antioxidant defenses and promotes protein oxidation in cerebral cortex of rats.

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N-acetylaspartic acid (NAA) is the biochemical hallmark of Canavan Disease, an inherited metabolic disease caused by deficiency of aspartoacylase activity. NAA is an immediate precursor for the enzyme-mediated biosynthesis of N-acetylaspartylglutamic acid (NAAG), whose concentration is also

Central Nervous System Symptoms Due to Transient Methemoglobinemia in a Child With G6PD Deficiency.

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The authors herein report a 5-year-old child who presented with massive hemolysis, irritability, and cyanosis. The final diagnosis was glucose-6-phosphate dehydrogenase deficiency with associated central nervous system symptoms probably because of concomitantly acquired methemoglobinemia following

UK malaria treatment guidelines.

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Malaria is the tropical disease most commonly imported into the UK, with 1500-2000 cases reported each year, and 10-20 deaths. Approximately three-quarters of reported malaria cases in the UK are caused by Plasmodium falciparum, which is capable of invading a high proportion of red blood cells and

The mitochondrial-targeted reactive species scavenger JP4-039 prevents sulfite-induced alterations in antioxidant defenses, energy transfer and cell death signaling in striatum of rats

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Sulfite oxidase (SO) deficiency is a disorder caused either by isolated deficiency of SO or by defects in the synthesis of its molybdenum cofactor. It is characterized biochemically by tissue sulfite accumulation. Patients present with seizures, progressive neurological damage and basal ganglia

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