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Regional activity of ornithine decarboxylase and edema formation after traumatic brain injury.
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This study examined ornithine decarboxylase (ODC) activity and edema formation bilaterally in brain cortices and hippocampi after lateral controlled cortical-impact injury in rats. To measure the activity of ODC, the brains of injured and control rats were frozen in situ at 30 minutes and at 6, 24,
Effect of difluoromethylornithine treatment on regional ornithine decarboxylase activity and edema formation after experimental brain injury.
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This study examined the effect of difluoromethylornithine (DFMO) on regional activities of ornithine decarboxylase (ODC) and edema formation in bilateral cerebral cortex and hippocampus after a unilateral controlled cortical-impact (CCI) injury in rats. To measure the activity of ODC, the brains of
Phorbol ester induction of 8-lipoxygenase in inbred SENCAR (SSIN) but not C57BL/6J mice correlated with hyperplasia, edema, and oxidant generation but not ornithine decarboxylase induction.
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Several responses suggested to be critical components of phorbol ester tumor promotion were compared in 12-O-tetradecanoylphorbol-13-acetate (TPA) promotion-sensitive SSIN and TPA promotion-resistant C57BL/6J mice. SSIN mice treated topically with 2 micrograms of TPA showed extensive hyperplasia
Intracranial Pressure Monitoring Demonstrates that Cerebral Edema Is Not Correlated to Hyperammonemia in a Child with Ornithine Transcarbamylase Deficiency.
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BACKGROUND
Ornithine transcarbamylase deficiency (OTCD) is an inborn error of urea cycle resulting in increased plasma levels of ammonia and glutamine and cerebral edema. However, the underlying mechanism of brain cytotoxicity remains controversial. Our objective is to present an unusual acute
L-ornithine-L-aspartate lowers plasma and cerebrospinal fluid ammonia and prevents brain edema in rats with acute liver failure.
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Brain edema sufficient to cause intracranial hypertension and brain herniation remains a major cause of mortality in acute liver failure (ALF). Studies in experimental animal models of ALF suggest a role for ammonia in the pathogenesis of both encephalopathy and brain edema in this condition. As
Ornithine decarboxylase activity and edema formation in cerebral ischemia of conscious gerbils.
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General anesthetic agents often affect the biochemical and physiologic changes triggered by cerebral ischemia. This study examined the regional activities of ornithine decarboxylase (ODC) in gerbils subjected to 5 min of bilateral carotid occlusion without anesthesia. At 2, 4, and 6 h of
Inhibition of 12-O-tetradecanoylphorbol-13-acetate-induced inflammatory skin edema and ornithine decarboxylase activity by theaflavin-3,3'-digallate in mouse.
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Among black tea polyphenols, theaflavins were generally considered to be the most effective in cancer chemoprevention. In this study, we examined the inhibitory effects of black tea polyphenols, including theaflavin (TF-1), a mixture (TF-2) of theaflavin-3-gallate and theaflavin-3'-gallate,
Fatal cerebral edema from late-onset ornithine transcarbamylase deficiency in a juvenile male patient receiving valproic acid.
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OBJECTIVE
The aims of this report are to 1) present a rare case of fatal cerebral edema associated with late-onset ornithine transcarbamylase (OTC) deficiency in a juvenile male patient receiving valproic acid and 2) review the neuropathologic changes associated with the hyperammonemia.
METHODS
Case
Prostratin, a nonpromoting phorbol ester, inhibits induction by phorbol 12-myristate 13-acetate of ornithine decarboxylase, edema, and hyperplasia in CD-1 mouse skin.
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Pretreatment of CD-1 mouse skin with prostratin (12-deoxyphorbol 13-acetate) inhibited biological response to phorbol 12-myristate 13-acetate. The three responses examined were hyperplasia, induction of ornithine decarboxylase, and edema; the characteristics of inhibition depended on the specific
Reduction in hyperammonaemia by ornithine phenylacetate prevents lipopolysaccharide-induced brain edema and coma in cirrhotic rats.
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OBJECTIVE
In liver failure, inflammation synergistically exacerbates the deleterious cerebral effects of ammonia. The aims were to test whether treatment with the ammonia-lowering agent ornithine phenylacetate (OP) and/or anti-TNF-α (infliximab) prevent the deleterious brain consequences of
Inhibition of ultraviolet-B radiation induced ornithine decarboxylase activity and edema formation by hydrolyzable and condensed tannins in mouse skin in vivo.
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Naturally occurring hydrolyzable (HT) and condensed (CT) tannins and their monomeric units were tested for their ability to inhibit the induction of epidermal ODC activity and the formation of skin edema by UVB, two responses that are linked to the hyperplastic and inflammatory components of skin
Ornithine transcarbamylase deficiency that developed at the age of 19 years with acute brain edema.
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A 19-year-old man had nausea, diarrhea, and general malaise the day before requesting emergency transport to his former primary physician. The patient became restless and had tonic seizures after admission. The patient was transferred to our hospital as there had been no improvement in his level of
Recurrent brain edema in ornithine-transcarbamylase deficiency.
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The induction of erythema, edema, and the polyamine synthesis enzymes ornithine decarboxylase and S-adenosyl-L-methionine decarboxylase in hairless mouse skin by psoralens and longwave ultraviolet light.
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Blockade of ornithine decarboxylase enzyme protects against ischemic brain damage.
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Polyamines are derived from ornithine by the actions of ornithine decarboxylase (ODC), which is the rate-limiting step in this pathway. Polyamines play a role in cell growth, neoplasia, differentiation, and response to injury. We have shown that transient cerebral ischemia gives rise to increased
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