cyanide/vefjadrep

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Pseudolaminar necrosis in cyanide intoxication: a neuropathology case report.

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We describe the gross and microscopic neuropathological changes in the brain of a 17-year-old male who died 4 days after being poisoned with cyanide. Previous reports indicate that following cyanide intoxication, the brain develops diffuse hypoxic/ischemic changes, predominantly of the basal

PPARalpha-mediated upregulation of uncoupling protein-2 switches cyanide-induced apoptosis to necrosis in primary cortical cells.

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Peroxisome proliferator-activated receptor alpha (PPARalpha) is a member of the nuclear factor PPAR family that regulates a variety of cellular functions, including lipid metabolism, cellular oxidative stress defense, and inflammatory responses. Based on the report that Wy14,643, a PPARalpha

Rubber Tree (Hevea brasiliensis) Bark Necrosis Syndrome III: A Physiological Disease Linked to Impaired Cyanide Metabolism.

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First attempts to discriminate between tapping panel dryness (TPD) and bark necrosis (BN), two Hevea sp. bark diseases leading to the cessation of latex production, showed differences in latex biochemical characteristics (1). Further, contrary to TPD, BN is characterized by inner phloem necrosis

Enhancement of cyanide-induced mitochondrial dysfunction and cortical cell necrosis by uncoupling protein-2.

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Uncoupling protein 2 (UCP-2) is expressed in the inner mitochondrial membrane and modulates mitochondrial function by partially uncoupling oxidative phosphorylation, and it has been reported to modulate cell death. Cyanide is a potent neurotoxin that inhibits complex IV to alter mitochondrial

Inducible nitric oxide synthase up-regulation and mitochondrial glutathione depletion mediate cyanide-induced necrosis in mesencephalic cells.

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We have previously shown in rat primary cultured mesencephalic cells that cyanide induces a high level of oxidative stress and necrotic death. To evaluate the mechanism of the cytotoxicity, the effects of cyanide on intracellular glutathione (GSH) pools and inducible nitric oxide synthase

Antibody-guided enzyme therapy of cancer producing cyanide results in necrosis of targeted cells.

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A number of enzyme/prodrug activation approaches for the treatment of cancer have been reported to date with varying success. We describe progress in the development of a system based on a beta-glucosidase enzyme in combination with a naturally occurring "prodrug," the sugar linamarin, which

Cyanide: an unreported cause of neurological complications following smoke inhalation.

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Although the combustion of natural and synthetic products can yield cyanide, its toxic role in residential fires is unclear. This case concerns a woman aged over 50 years who presented comatose, pulseless and apnoeic after a domestic fire. Cardiopulmonary resuscitation and on-site administration of

Role for tumor necrosis factor alpha receptor 1 and interleukin-1 receptor in the suppression of mouse hepatocyte apoptosis by the peroxisome proliferator nafenopin.

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Peroxisome proliferators (PPs) cause rodent liver enlargement and tumors. In vitro, PPs induce rat and mouse hepatocyte DNA synthesis and suppress apoptosis, a response mimicked by exogenous tumor necrosis factor alpha (TNFalpha). Here, we determine the role of TNF receptor 1 (TNFR1), TNF receptor 2

Aptamer-based determination of tumor necrosis factor α using a screen-printed graphite electrode modified with gold hexacyanoferrate.

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An aptamer based method is presented for the voltammetric determination of human tumor necrosis factor alpha (TNF-α). Layers of gold hexacyanoferrate (AuHCF) and gold nanoparticles (AuNPs) were directly immobilized on a graphite screen-printed electrode (SPE). Through the strong interaction between

A Lipid Base Formulation for Intramuscular Administration of a Novel Sulfur Donor for Cyanide Antagonism.

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This study represents a new formulation of the novel Cyanide (CN) antidote, Dimethyl trisulfide (DMTS), for intramuscular administration. This is a naturally occurring organosulfur molecule with the capability of reacting with CN more efficiently than the present sulfur donor type CN therapy of

Chronic cyanide poisoning of rainbow trout and its effects on growth, respiration, and liver histopathology.

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Cyanide markedly affected growth and resting metabolic rate while causing degenerative hepatic necrosis in juvenile rainbow trout (Salmo gairdneri, Richardson). This was revealed during two experiments performed in continuously renewed water at 12.5 degree C with fish fed a restricted artificial

Intraosseous versus intravenous infusion of hydroxocobalamin for the treatment of acute severe cyanide toxicity in a Swine model.

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OBJECTIVE Easily administrated cyanide antidotes are needed for first responders, military troops, and emergency department staff after cyanide exposure in mass casualty incidents or due to smoke inhalation during fires involving many victims. Hydroxocobalamin has proven to be an effective antidote,

Differential susceptibility of brain areas to cyanide involves different modes of cell death.

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We have demonstrated that cyanide (KCN) induces selective degeneration of dopaminergic neurons in mice and apoptotic cell death in cultured neurons. In the present study the mode of cyanide-induced cell death was determined in the susceptible brain areas. Mice were treated with KCN (6 mg/kg ip) or

Alteration of respiration capacity and transcript accumulation level of alternative oxidase genes in necrosis lines of common wheat.

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Mitochondrial alternative oxidase (AOX) is the terminal oxidase responsible for cyanide-insensitive and salicylhydroxamic acid-sensitive respiration in plants. AOX is a key enzyme of the alternative respiration pathway. To study the effects of necrotic cell death on the mitochondrial function,

Cyanide encephalopathy following therapy with sodium nitroprusside: report of a case.

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Bilateral necrosis of the globus pallidus was observed in a 43-year-old man who had received treatment for malignant hypertension with sodium nitroprusside. Cyanide released from sodium nitroprusside may have caused the pallidal lesions in the presence of deranged liver function and episodes of

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