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malic enzyme/sarcoma
Odkaz sa uloží do schránky
5 výsledky
Glucocorticoid-dependent induction of HMG-CoA reductase and malic enzyme gene expression by polychlorinated biphenyls in rat hepatocytes.
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Administration of xenobiotics to rats results in hypercholesterolemia and in the induction of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and malic enzyme. To investigate the mechanism of the induction of the enzymes by xenobiotics, the effects of xenobiotics on gene expressions for
Tumor-induced alterations in hepatic malic enzyme and carnitine palmitoyltransferase activity.
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To better understand the role of the liver in the hypertriglyceridemia observed in a tumor-bearing state, we have examined tumor-induced alterations in hepatic lipogenesis and fatty acid oxidation. The effects of differing tumor burden as well as tumor excision on the activity and mRNA levels of
The possible role of TNF-alpha and IL-2 in inducing tumor-associated metabolic alterations.
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This study was conducted to investigate the role of tumor necrosis factor-alpha (TNF-alpha) and interleukin-2 (IL-2) in inducing cancer cachexia, and the results were compared with those obtained from our previous study on Fisher 344 rats with methylcholanthrene-induced sarcoma. Three groups of male
The effects of a biological response modifier, OK-432, on tumor-induced alterations in the host metabolism.
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The effects of multicytokine inducer, OK-432, on tumor-induced metabolic alterations were studied by assessing three key regulatory enzymes of gluconeogenesis, de novo fatty acid synthesis and the triglyceride clearance pathways. Two Klinish Einheit (KE) of OK-432 was subcutaneously injected on
Sheep gene mapping: additional DNA markers included (CASB, CASK, LALBA, IGF-1 and AMH).
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DNA extracted from 25 hamster-sheep hybrid cell lines was subjected, after Southern blotting, to hybridization with CASB, CASK, LALBA, IGF-1 and AMH cDNA probes. CASB and CASK segregated together and IGF-1 and LALBA were found syntenic with the LDHB-PEPB-TPI-GAPD-SHMT-KRTB group. No other synteny
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