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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Archives of environmental contamination and toxicology 24 (1993), S. 120-120 
    ISSN: 1432-0703
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering , Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Archives of environmental contamination and toxicology 21 (1991), S. 505-513 
    ISSN: 1432-0703
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering , Medicine
    Notes: Abstract Model ecosystems, simulating a Baltic Sea littoral habitat, were used for evaluating the effects of different effluents from kraft pulp mill industries on fish. Populations of newly hatched three-spined stickleback (Gasterosteus aculeatus) were continuously exposed to four different types of pulp mill effluents in a flowthrough sea water system. After 51/2 months of exposure, the sticklebacks were collected for a skin parasite count and histological examination of the gills and liver. The frequencies of two types of skin-dwelling ciliates of the generaTrichodina andApiosoma were higher in the exposed fish populations, particularly in those exposed to the high effluent doses (diluted 400 times). Anomalies in the liver cell structure were observed as necrotic cells, nuclear pyknosis, vacuolation, and fat accumulation. The two effluents from the factories producing unbleached softwood and bleached hardwood without oxygen pre-bleaching affected the sticklebacks most, both in respect to ciliate abundance and to liver anomalies.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-4919
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Summary Approximately 2% of the proteins solubilised from rat liver microsomes or rapidly sedimenting endoplasmic reticulum (RS-ER) adsorbed to poly(A)-Sepharose. The adsorption appeared to be selective for a few proteins, and proteins of different apparent molecular weights adsorbed from RS-ER and the microsomes. The proteins from RS-ER with affinity for poly(A) were coupled to Sepharose and used for the purification of mRNA from rabbit mammary glands. A portion of the RNA which did not adsorb to poly(U)-Sepharose adsorbed to protein-Sepharose and was active in a cell-free protein synthesis system.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Molecular and cellular biochemistry 193 (1999), S. 119-125 
    ISSN: 1573-4919
    Keywords: benzamides ; nicotinamides ; apoptosis ; inflammation ; NF-kB ; DNA repair
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Our laboratory has concentrated on the possible regulation the benzamides and nicotinamides may have on the processes of DNA repair and apoptosis. Recent reports [14-16] have suggested that both apoptosis and inflammation are regulated by the transcription factor NF-kB. We have initiated studies regarding the hypothesis that the benzamides and nicotinamides could inhibit the production of tumor necrosis factor alpha (TNFalpha) and the inflammatory response as well as induce apoptosis via inhibition of NF-kB. Our data have shown that nicotinamide and two N-substituted benzamides, metoclopramide (MCA) and 3-chloroprocainamide (3-CPA), gave dose dependent inhibition of lipopolysacharide induced TNFalpha in the mouse within the dose range of 10-500 mg/kg. Moreover, lung edema was prevented in the rat by 3 ï 50 mg/kg doses of 3-CPA or MCA, and 100-200 μM doses of MCA could also inhibit NF-kB in Hela cells. Taken together these data strongly support the notion that benzamides and nicotinamides have potent anti-inflammatory and antitumor properties, because their primary mechanism of action is regulated by inhibition at the gene transcription level of NF-kB, which in turn inhibits TNFalpha and induces apoptosis.
    Type of Medium: Electronic Resource
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