cystine/seizures

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High expression of cystine-glutamate antiporter xCT (SLC7A11) is an independent biomarker for epileptic seizures at diagnosis in glioma.

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Epileptic seizures are an important cause of morbidity in glioma patients. Substantial lines of evidence support the concept of the excitatory neurotransmitter glutamate being a crucial mediator of glioma-associated seizures. In gliomas, non-vesicular secretion of glutamate via the cystine-glutamate

Plasma cysteine/cystine redox couple disruption in animal models of temporal lobe epilepsy.

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Currently the field of epilepsy lacks peripheral blood-based biomarkers that could predict the onset or progression of chronic seizures following an epileptogenic injury. Thiol/disulfide ratios have been shown to provide a sensitive means of assessing the systemic redox potential in tissue and

Cystinosis. Intracellular cystine depletion by aminothiols in vitro and in vivo.

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Certain aminothiols rapidly deplete cultured cystinotic skin fibroblasts of their abnormally high free (nonprotein) cystine pool. The free cystine content of these cells if reduced by over 90% in 1 h with 0.1 mM cysteamine. This is more rapid than previously known methods of removing free cystine

Does Tc-99m ECD ictal brain SPECT have incremental value in localization of epileptogenic zone and predicting postoperative seizure freedom in cases with discordant video electroencephalogram and MRI findings?

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Objective: Localization of epileptogenic focus in drug-refractory epilepsy using Tc-99m ethylene cystine dimer (ECD) brain single photon emission computed tomography (SPECT) is less studied in patients with discordant findings on video

Does Tc-99m ECD ictal brain SPECT have incremental value in localization of epileptogenic zone and predicting postoperative seizure freedom in cases with discordant video electroencephalogram and MRI findings?

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Cystine neurotoxicity is increased by taurine deficiency.

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In an attempt to increase taurine biosynthesis in cats fed a taurine-free diet we supplied an excess of the precursor, cystine, in the diet. All nine cats exhibited extreme signs of neurotoxicity including lethargy, inability to stand, rigidity of the neck and lower limbs, absence and epileptic

SLC7A11 expression is associated with seizures and predicts poor survival in patients with malignant glioma.

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Glioma is the most common malignant primary brain tumor. Its rapid growth is aided by tumor-mediated glutamate release, creating peritumoral excitotoxic cell death and vacating space for tumor expansion. Glioma glutamate release may also be responsible for seizures, which complicate the clinical

Genetic and pharmacological manipulation of glial glutamate transporters does not alter infection-induced seizure activity.

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The contribution of glial transporters to glutamate movement across the membrane has been identified as a potential target for anti-seizure therapies. Two such glutamate transporters, GLT-1 and system x_c^-, are expressed on glial cells, and modulation of their expression and

Seizures and gliomas--towards a single therapeutic approach.

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Epilepsy often develops in patients with glioma, and the two conditions share common pathogenic mechanisms. Altered expression of glutamate transporters, including the cystine-glutamate transporter (xCT) system, increases concentrations of extracellular glutamate, which contribute to epileptic

Compromised glutamate transport in human glioma cells: reduction-mislocalization of sodium-dependent glutamate transporters and enhanced activity of cystine-glutamate exchange.

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Elevated levels of extracellular glutamate ([Glu](o)) can induce seizures and cause excitotoxic neuronal cell death. This is normally prevented by astrocytic glutamate uptake. Neoplastic transformation of human astrocytes causes malignant gliomas, which are often associated with seizures and

Loss of system x(c)- does not induce oxidative stress but decreases extracellular glutamate in hippocampus and influences spatial working memory and limbic seizure susceptibility.

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System x(c)- exchanges intracellular glutamate for extracellular cystine, giving it a potential role in intracellular glutathione synthesis and nonvesicular glutamate release. We report that mice lacking the specific xCT subunit of system x(c)- (xCT(-/-)) do not have a lower hippocampal glutathione

[Sulfite oxidase activity deficiency caused by cofactor molybdenum deficiency: A case of early severe encephalopathy].

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Neonatal seizure incidence is approximately 3.5/1000 live births. Inborn metabolic diseases account for approximately 1-4% of neonatal seizure cases. Among them, the catabolism anomaly of sulfite to sulfate caused by sulfite oxidase or cofactor molybdenum deficiency (MoCD) is a rare metabolic

Isolated sulfite oxidase deficiency.

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Isolated sulfite oxidase (SO) deficiency is an autosomal recessively inherited inborn error of sulfur metabolism. In this report of a ninth patient the clinical history, laboratory results, neuropathological findings and a mutation in the sulfite oxidase gene are described. The data from this

Infantile isolated sulphite oxidase deficiency in a Chinese family: a rare neurodegenerative disorder.

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We report the clinical, biochemical, neuroradiological, and neurophysiological findings of a 4-year-old Chinese girl with infantile isolated sulphite oxidase deficiency. This is the first reported case in our locality. She presented at the age of 5 months with refractory seizures and developmental

Biochemistry of homocysteine in health and diseases.

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The amino acid homocysteine (Hcy), formed from methionine has profound importance in health and diseases. In normal circumstances, it is converted to cysteine and partly remethylated to methionine with the help of vit B12 and folate. However, when normal metabolism is disturbed, due to deficiency of

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