[Protracted dinitrophenol liver glycogenosis and phenomena of glycogen storage in experimental liver cirrhosis].
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Reparative regeneration after fetal tissue transplantation and after surgical stimulation was studied in rats with experimental cirrhosis of the liver. Fetal tissue restored the morphology and function of cirrhotic liver and modified functional activity of peritoneal macrophages.
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Liver cirrhosis is a very common illnesses and currently its treatment remains unpromising. In a research line devoted to studying the hepatotoxicity of certain substances we have evaluated the lesions that appear prior to the occurrence of cirrhosis and hepatocarcinoma in order to test, in different assays liver-protecting substances such as cyanidanol-3 that have been seen to lead to an improvement in morphological alterations in the liver and even to reverse such lesions. The mechanisms of action of this compound are discussed. The authors believe that considerable work remains to be carried out but that some day some liver-protecting substances that yield good experimental results may be applied to clinical situations.
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Accelerated telomere loss has been proposed to be a factor leading to end-stage organ failure in chronic diseases of high cellular turnover such as liver cirrhosis. To test this hypothesis directly, telomerase-deficient mice, null for the essential telomerase RNA (mTR) gene, were subjected to genetic, surgical, and chemical ablation of the liver. Telomere dysfunction was associated with defects in liver regeneration and accelerated the development of liver cirrhosis in response to chronic liver injury. Adenoviral delivery of mTR into the livers of mTR(-/-) mice with short dysfunctional telomeres restored telomerase activity and telomere function, alleviated cirrhotic pathology, and improved liver function. These studies indicate that telomere dysfunction contributes to chronic diseases of continual cellular loss-replacement and encourage the evaluation of "telomerase therapy" for such diseases.
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