ornithine/seizures

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Induction of ornithine decarboxylase as a possible mediator of seizure-elicited changes in genomic expression in rat hippocampus.

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Small electrolytic lesions placed in the hilus of the dentate gyrus have been shown to induce behavioral seizures, an elevation in the concentration of the opioid peptide enkephalin, and an increase in the transcription of the gene coding for the peptide precursor of enkephalin. Since polyamines and

Enhanced endogenous ornithine concentrations protect against tonic seizures and coma in acute ammonia intoxication.

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Pretreatment of mice with 5-fluoromethylornithine (5FMOrn), a selective inactivator of ornithine aminotransferase, diminishes the accumulation of ammonia in the brain after administration of ammonium acetate, and antagonizes ammonia-induced fatal tonic extensor convulsions. In about 50% of the

Ornithine decarboxylase induction and polyamine synthesis in the kindling of seizures: the effect of alpha-difluoromethylornithine.

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It has been suggested that the kindling of seizures may depend on the induction of genes encoding enzymes involved in neurotransmission. Experimental seizures are followed by an especially rapid and massive induction of brain ornithine decarboxylase (ODC), an enzyme which catalyses the rate-limiting

Protective effect of NG-nitro-L-arginine (N5-[imino(nitroamino)methyl]-L-ornithine) against cyanide-induced convulsions in mice.

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The effects of NG-nitro-L-arginine (NNA; an inhibitor of the oxidative L-arginine pathway) on convulsions induced by cyanide were investigated in mice. NNA prevented cyanide-induced convulsions in a dose-dependent manner. Furthermore, the inhibitory effect against convulsions induced by cyanide with

Induction of immediate early genes, interleukin-1 beta and ornithine decarboxylase messenger RNA in spinal cord by seizures.

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Fatal hyperammonaemia due to late-onset ornithine transcarbamylase deficiency.

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In this case report we describe a 67-year-old male, admitted to the ICU with pneumonia who unexpectedly developed a fatal coma due to hyperammonaemia. At postmortem the diagnosis late-onset ornithine transcarbamylase deficiency was made. The non-specific clinical presentation, the rapid

Evidence for cholinergic neuronal loss in brain in congenital ornithine transcarbamylase deficiency.

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Congenital ornithine transcarbamylase (OTC) deficiency in humans is associated with seizures and mental retardation. As part of a series of studies to delineate the neurochemical features of OTC deficiency, activities of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE), respectively,

Repeated electroconvulsive shock increases glial fibrillary acidic protein, ornithine decarboxylase, somatostatin and cholecystokinin immunoreactivities in the hippocampal formation of the rat.

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Rats were submitted to single or repeated (7 days, one session for each day) sessions of electroconvulsive shock. A computer-assisted morphometric and microdensitometric analysis of glial fibrillary acidic protein-, ornithine decarboxylase-, somatostatin- and cholecystokinin-like immunoreactivities

Transcriptional activation of ornithine decarboxylase in adult and neonatal hippocampal slices.

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Ornithine decarboxylase (ODC) is the rate-limiting enzyme in polyamine synthesis and is regulated by both transcription-dependent and transcription-independent mechanisms. We compared the effects of asparagine, an amino acid previously shown to increase ODC activity in adult hippocampal slices, on

Adult Presentation of Ornithine Transcarbamylase Deficiency: 2 Illustrative Cases of Phenotypic Variability and Literature Review.

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Ornithine transcarbamylase (OTC) deficiency is an X-linked recessive disorder that usually presents in the neonatal period. Late-onset presentation of OTC can cause mild to severe symptoms. We describe laboratory and clinical findings of late-onset presentations of OTC deficiency. We conducted a

Evidence for forebrain cholinergic neuronal loss in congenital ornithine transcarbamylase deficiency.

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Congenital ornithine transcarbamylase (OTC) deficiency in humans results in failure to thrive, hypotonia, seizures and mental retardation. Neuropathologic evaluation reveals significant cerebral cortical atrophy, delayed myelination and Alzheimer type II astrocytosis. Using an animal model of

Ornithine Transcarbamylase Deficiency: If at First You Do Not Diagnose, Try and Try Again.

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Ornithine transcarbamylase (OTC) deficiency is well known for its diagnosis in the neonatal period. Presentation often occurs after protein feeding and manifests as poor oral intake, vomiting, lethargy progressing to seizure, respiratory difficulty, and eventually coma. Presentation at adulthood is

A lethal neonatal variant of carbamoyl-phosphate synthetase deficiency in combination with an intermediate activity of L-ornithine: 2-oxoglutarate amino-transferase.

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Shortly after birth, a newborn girl developed anorexia, hypotonia, apneic attacks and seizures. After 61 h the child died in coma. Biochemically, a highly elevated blood ammonia level was found together with an increased plasma level of the amino acids mainly involved in ammonia detoxication. Enzyme

[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

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