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isonicotinic acid/nekrose
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8 resultater
[Intrauterine fetal necrosis due to the use of isonicotinic acid hydrazide in pregnant women].
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[Drug prophylaxis of liver lesions induced by isoniazid and its metabolites].
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The results of the experiments with use of isoniazid and its metabolites showed that in the liver of rats isoniazid induced albuminous degeneration with stroma inflammation and hepatocyte necrosis, monoacetylhydrazine induced fatty hepatosis, acetylisoniazid induced fatty hepatosis with stroma
[Acute poisoning with selected hepatotoxic agents: biochemistry of toxic effect, clinical symptoms and treatment].
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The paper discusses etiopathogenesis, clinical symptoms and treatment in acute poisoning with hepatotoxic agents. The liver is a critical organ in acute poisoning with Amanita phalloides, carbon tetrachloride, iron compounds and isonicotinic acid hydrazide. Based on literature reports and own
Changes of lymph metabolites in a rat model of sepsis induced by cecal ligation and puncture.
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BACKGROUND
Sepsis is a clinical syndrome defined by a systemic response to infection and remains a prevalent clinical challenge. The underlying pathophysiology of sepsis is poorly understood. Using a metabolomic method, the present study observed changes in lymph composition during sepsis in a
Activation of hsr203, a plant gene expressed during incompatible plant-pathogen interactions, is correlated with programmed cell death.
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hsr203J is a tobacco gene whose activation is rapid, highly localized, and specific for incompatible interactions between tobacco and the bacterial pathogen Ralstonia solanacearum. The effect of other hypersensitive response (HR)-inducing pathogens and elicitors has been tested with transgenic
Isoniazid hepatoxicity: the relationship between covalent binding and metabolism in vivo.
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The relationship between the hepatotoxicity and metabolism of isoniazid and its metabolites, acetylisoniazid and acetylhydrazine, has been investigated. Toxic doses of acetylisoniazid and acetylhydrazine, radiolabeled in the acetyl group, were found to bind covalently to liver protein in vivo. This
Hepatotoxicity and metabolism of iproniazid and isopropylhydrazine.
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Iproniazid (1-isonicotinoyl-2-isopropylhydrazine), an antidepressant drug removed from clinical use because of hepatic injury, and isopropylhydrazine, a metabolite of iproniazid, were found to be potent hepatotoxins in rats. This animal model was used in studies in vivo and in vitro to define better
Isoniazid liver injury: clinical spectrum, pathology, and probable pathogenesis.
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The clinical spectrum of isoniazid-induced liver injury seems to be clinically, biochemically, and histologically indistinguishable from viral hepatitis, except that the injury occurs primarily in persons older than 35 years. A possible relation between susceptibility of patients to isoniazid liver
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