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  • 1
    Electronic Resource
    Electronic Resource
    Increases in tumor necrosis factor-α following transient global cerebral ischemia do not contribute to neuron death in mouse hippocampus (2005)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 93 (2005), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The actions of tumor necrosis factor-α (TNF-α) produced by resident brain cells and bone marrow-derived cells in brain following a transient global ischemia were evaluated. In wild-type mice (C57Bl/6J) following 20 min ischemia with bilateral common carotid artery occlusion (BCCAo), TNF-α mRNA expression levels in the hippocampus were significantly increased at 3 h and 36 h and exhibited a biphasic expression pattern. There were no hippocampal TNF-α mRNA expression levels at early time points in either wild-type mice bone marrow transplanted (BMT)-chimeric-TNF-α gene-deficient (T/W) or TNF-α gene-deficient mice BMT-TNF-α gene-deficient mice (T/T), although TNF-α mRNA levels were detectable in T/W BMT mice at 36 h. Histopathological findings showed no intergroup differences between wild-type and TNF-α gene-deficient mice at 4 and 7 days after transient ischemia. In addition, nuclear factor-κB (NF-κB) was activated within 12 h after global cerebral ischemia, but electrophoretic mobility shift assays (EMSA) showed no intergroup differences between wild type and TNF-α gene-deficient mice. In summary, early hippocampal TNF-α mRNA expression may not be related to bone marrow-derived cells, and secondary TNF-α expression as early as 36 h after ischemia probably resulted mainly from endogenous brain cells and possibly a few bone marrow-derived cells. Although we cannot exclude the possibility of the TNF-α contribution to the physiologic changes of hippocampus after transient global ischemia, these results indicate that TNF-α does not influence the morphological changes of the hippocampal neurons under our study condition.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.2005.03163.x
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  • 2
    Electronic Resource
    Electronic Resource
    EFFECTS OF ADRENALINE INFUSION ON PLASMA LIPIDS AND NORADRENALINE LEVELS IN RABBITS WITH ADRIAMYCIN-INDUCED CARDIOMYOPATHY (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 24 (1997), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. We investigated the acute effects of adrenaline infusion on plasma lipid levels in vehicle- and adriamycin-treated rabbits. Lipids were measured before and 30 and 60 min after the commencement of continuous intravenous administration of adrenaline (0.06 |xg/kg per min) or saline in pentobarbital-anaesthetized rabbits.2. Adrenaline infusion significantly increased plasma free fatty acid (P 〈 0.05) and noradrenaline (NA) levels (P 〈 0.05) in vehicle-treated control rabbits, but not in adriamycin-treated rabbits. However, adrenaline had no effect on plasma total cholesterol, free cholesterol, high-density lipoprotein-cholesterol, triglyceride or phospholipid levels.3. Pretreatment with propranolol almost completely inhibited increased plasma free fatty acid and NA levels associated with adrenaline infusion, suggesting that adrenaline increases plasma free fatty acid and NA levels via the stimulation of p-adreno-ceptors in vehicle-treated rabbits.4. It is suggested that both the production of plasma free fatty acids and the release of NA via the activation of β-adrenoceptors is reduced in rabbits with adriamycin-induced cardiomyopathy. This may be related to the down-regulation of β-adrenoceptors caused by elevated plasma NA levels induced by cardiac failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1997.tb01230.x
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  • 3
    Electronic Resource
    Electronic Resource
    Impaired synthesis of retinol-binding protein and transthyretin in rat liver with bile duct obstruction (1996)
    Springer
    Digestive diseases and sciences 41 (1996), S. 1038-1042 
    Details
    ISSN: 1573-2568
    Keywords: cholestasis ; retinol-binding protein ; transthyretin ; mRNA ; polysome ; protein synthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To gain further insight into the protein metabolism in bile duct-obstruction, we examined the synthesis of retinol-binding protein (RBP) and transthyretin (TTR) in rats with common bile duct-ligation. In these rats, liver and plasma levels of RBP and TTR decreased markedly, whereas liver retinoid contents remained unchanged. Although there appeared no decrease in the total amount of RBP or TTR mRNA expressed in the liver, the subcellular distribution of these mRNAs changed from the membrane-bound polysome fraction to the membrane-unbound polysome fraction. This abnormal distribution recovered rapidly after biliary drainage, resulting in the subsequent recovery of the plasma RBP and TTR levels. These observations suggest that cholestasis inhibits the synthesis and secretion of RBP and TTR by disrupting the binding of their mRNAs to membrane-bound polysomes. Plasma levels of RBP and TTR might be sensitive indicators of the recovery of protein synthesis after biliary drainage in patients with obstructive biliary disorders.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02091549
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    Paper (German National Licenses)
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