177 research outputs found

    Pulmonary metastases radiologic imaging and pathologic correlation

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    The main problem in the treatment of pulmonary lymphangioleiomyomatosis, which frequently occurs in the reproductive age, is the control of chylothorax and disease progression. We herein report a case of a 62-year-old woman who underwent surgery for recurrent chylothorax. Histologic examination of lung and lymph node biopsies demonstrated lymphangioleiomyomatosis. Thirty-six months after tetracycline pleurodesis and high-dose medroxyprogesterone acetate therapy, the disease was stable and chylothorax effectively controlled. It would therefore appear that hormonal treatment with medroxyprogesterone acetate may be beneficial in postmenopausal wome

    In vivo interaction of lead with aminolevulinic acid dehydratase and induction of a thermolabile factor: an experimental model.

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    Aminolevulinic acid dehydratase (ALA-D) activity of male albino Wistar rats was used as an experimental model for a study on the interaction of lead with biological systems. Lead at 1 mg/kg was administered i.p. and the rats were killed immediately, and at 30 min, 1, 2, 3, and 4 h after treatment. It was shown that lead (Pb) interacted directly with the enzyme molecule immediately after treatment, first on the active site of zinc (Zn) and then on the thiolic groups. Induction of the so-called thermolabile factor (TF) seemed to occur later, i.e., it may only be shown from the 2nd-3rd h after treatment. The long-term persistence of lead-induced TF in the acute phase of intoxication may be the key to the interpretation of some chronic toxic effects

    Heating reactivation of rats aminolevulinic acid dehydratase in lead poisoning.

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    Heat reactivation (60 degrees C for 5 minutes) of the red blood cells aminolevulinic acid dehydratase activity was studied in lead treated rats (0.25 to 5.0 mg/kg b.w., i.p., for 4 weeks). Complete enzyme reactivation occurs with lead blood concentration up to about 70 mcg/dl. At higher blood lead concentrations, only a part of the enzyme can be restored by heating. The different mechanisms of aminolevulinic acid dehydratase activity inhibition by lead are discussed

    Liver toxicity due to 1,2-dichloropropane in the rat.

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    The effect of 1,2-dichloropropane on rat liver was studied after short (5 days) and long term (4 weeks) i.p. administration. Animals were injected daily with 10-500 mg/kg body wt 1,2-dichloropropane and biochemical and histological changes of liver were investigated. Treatment was monitored by measuring urinary mercapturic acid excretion. A significant increase of mercapturate excretion was observed at all dose levels, with no further increase during the treatment; at lower doses a return to baseline values occurred within 48 h after the end of treatment. Mercapturate excretion at the end of weeks 2, 3 and 4 of treatment was significantly lower than that observed at the end of week 1. The liver reduced glutathione content was different after single or repeated injections. A dose-dependent decrease of liver reduced glutathione was observed after a single injection and a dose-dependent increase after 4 weeks. The liver biochemical pattern after 4 weeks of treatment (characterized by a decrease of cytochrome P-450 and by an increase of reduced glutathione and glutathione S-transferase activity) suggests a hyperplastic evolution of the liver cells, probably a repair mechanism induced by early depletion of reduced glutathione. Light microscopy confirms that the prevalent alterations are regenerative in type (atypical mitosis and hyperplastic nodules). Areas of focal necrosis are isolated, and trend to disappear after long term treatment
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