guanine/פרכוס אפילפטי

הקישור נשמר בלוח

מאמריםניסויים קלינייםפטנטים

בחר סוג מיון

עמוד 1 מ 77 תוצאות

[Partial deficiency of hypoxanthine-guanine phosphoribosyltransferase presenting seizure and psychomotor retardation: a case report].

רק משתמשים רשומים יכולים לתרגם מאמרים

התחבר הרשם

An 18-year-old man was admitted to our hospital because of convulsive seizure. He had psychomotor retardation and intellectual disability from childhood, and had been diagnosed with attention deficit-hyperactivity disorder when he was 12 years old. He showed mental deficit (Wechsler Adult

Intracerebroventricular guanine-based purines protect against seizures induced by quinolinic acid in mice.

רק משתמשים רשומים יכולים לתרגם מאמרים

התחבר הרשם

Acute and chronic administration of the nucleoside guanosine have been shown to prevent quinolinic acid (QA) and alpha-dendrotoxin-induced seizures, as well as to impair memory and anxiety in rats and mice. In this study, we investigated the effect of i.c.v. administration of guanine-based purines

Quinolinic acid-induced seizures stimulate glutamate uptake into synaptic vesicles from rat brain: effects prevented by guanine-based purines.

רק משתמשים רשומים יכולים לתרגם מאמרים

התחבר הרשם

Glutamate uptake into synaptic vesicles is a vital step for glutamatergic neurotransmission. Quinolinic acid (QA) is an endogenous glutamate analog that may be involved in the etiology of epilepsy and is related to disturbances on glutamate release and uptake. Guanine-based purines (GBPs) guanosine

[A novel mutation in KCNQ2 gene causes benign familial infantile convulsions (BFIC) in a Chinese family].

רק משתמשים רשומים יכולים לתרגם מאמרים

התחבר הרשם

OBJECTIVE Benign familial infantile convulsions (BFIC) is a form of idiopathic epileptic syndrome characterized by onset of afebrile seizures between 3 and 12 months of life, Spontaneous remission after several weeks or months, and autosomal dominant mode of inheritance. Previous linkage analysis in

Guanosine and GMP prevent seizures induced by quinolinic acid in mice.

רק משתמשים רשומים יכולים לתרגם מאמרים

התחבר הרשם

In the mammalian CNS, glutamate and GABA are the principal neurotransmitters mediating excitatory and inhibitory synaptic events, respectively, and have been implicated in the neurobiology of seizures. Guanine-based purines, including the nucleoside guanosine and the nucleotide GMP, have been shown

Epileptic Encephalopathy Caused by Mutations in the Guanine Nucleotide Exchange Factor DENND5A.

רק משתמשים רשומים יכולים לתרגם מאמרים

התחבר הרשם

Epileptic encephalopathies are a catastrophic group of epilepsies characterized by refractory seizures and cognitive arrest, often resulting from abnormal brain development. Here, we have identified an epileptic encephalopathy additionally featuring cerebral calcifications and coarse facial features

Seizure progression triggered by IQSEC3 loss is mitigated by reducing activated microglia in mice

רק משתמשים רשומים יכולים לתרגם מאמרים

התחבר הרשם

IQSEC3, a guanine nucleotide exchange factor for ADP-ribosylation factors (ARF-GEFs) is specifically expressed at GABAergic synapses, and its loss increases seizure susceptibility in mice. However, the contribution of microglia to initiation and/or progression of seizures in IQSEC3-deficient mice

Stimulatory guanine nucleotide binding protein subunit 1 mutation in two siblings with pseudohypoparathyroidism type 1a and mother with pseudopseudohypoparathyroidism.

רק משתמשים רשומים יכולים לתרגם מאמרים

התחבר הרשם

Pseudohypoparathyroidism (PHP) type la is characterized by multihormone resistance and a constellation of somatic features referred to as Albright hereditary osteodystrophy. Several mutations in the gene coding for the Gs alpha subunit (GNAS1) have been described. Clinical symptoms are heterogeneous

Allopurinol-induced arteritis in partial HGPRTase deficiency. Atypical seizure manifestation.

רק משתמשים רשומים יכולים לתרגם מאמרים

התחבר הרשם

A 17-year-old boy with partial hypoxanthine-guanine phosphoribosyl transferase deficiency developed a hypersensitivity reaction to allopurinol. The reaction was manifested by the development of bizarre, atypical seizures. The patient had been neurologically normal prior to the reaction. Seizures

Cerebrospinal fluid purine metabolite and neuron-specific enolase concentrations after febrile seizures.

רק משתמשים רשומים יכולים לתרגם מאמרים

התחבר הרשם

If febrile seizures cause significant compromise of neuronal metabolism (whether permanent or reversible), this should be reflected in an increase in the cerebrospinal fluid concentrations of neuron-specific enolase (NSE) and/or adenosine triphosphate (ATP) breakdown products. In the present study,

Purine metabolites and pyrimidine bases in cerebrospinal fluid of children with simple febrile seizures.

רק משתמשים רשומים יכולים לתרגם מאמרים

התחבר הרשם

Adenosine monophosphate, inosine monophosphate, inosine, adenosine, guanosine, adenine, guanine, hypoxanthine, xanthine, uric acid and pyrimidine bases were determined in the CSF of 18 children after simple febrile seizures and in a control group. There was no statistically significant difference

Cerebrospinal fluid purine metabolites after complex febrile convulsions.

רק משתמשים רשומים יכולים לתרגם מאמרים

התחבר הרשם

Adenosine monophosphate, inosine monophosphate, inosine, adenosine, guanosine, adenine, guanine, hypoxanthine, xanthine and uric acid were determined in cerebrospinal fluid (CSF) of 15 children after complex febrile seizures (CFS) and in 27 after simple febrile seizures (SFS), and compared with

Cerebrospinal fluid purine metabolites and pyrimidine bases after brief febrile convulsions.

רק משתמשים רשומים יכולים לתרגם מאמרים

התחבר הרשם

Adenosine monophosphate, inosine monophosphate, inosine, adenosine, guanosine, adenine, guanine, hypoxanthine, xanthine, uric acid, and pyrimidines bases were determined in cerebrospinal fluid (CSF) of 52 children after simple febrile seizures and in a control group of 63 children. There was no

Guanine nucleotides are competitive inhibitors of N-methyl-D-aspartate at its receptor site both in vitro and in vivo.

רק משתמשים רשומים יכולים לתרגם מאמרים

התחבר הרשם

Guanine nucleotides were shown to alter N-methyl-d-aspartate (NMDA) receptor-effector coupling by competitive antagonism at the glutamate binding site, rather than via interaction with an intracellularly located GTP-binding protein. Thus, in contrast to known G-protein linked receptors, micromolar

Electrophysiological effects of guanosine and MK-801 in a quinolinic acid-induced seizure model.

רק משתמשים רשומים יכולים לתרגם מאמרים

התחבר הרשם

Quinolinic acid (QA) is an N-methyl-D-aspartate receptor agonist that also promotes glutamate release and inhibits glutamate uptake by astrocytes. QA is used in experimental models of seizures studying the effects of overstimulation of the glutamatergic system. The guanine-based purines (GBPs),

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Herbal & Natural Medicine

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