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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 22 (1966), S. 664-664 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Riassunto Vengono presentati alcuni dati che dimostrano come sostanze che abbassino il livello degli FFA plasmatici nei ratti diminuiscano anche il livello dei corpi chetonici. Viene discussa la possibilità che la formazione dei corpi chetonici possa dipendere dal controllo della liberazione degli FFA nel tessuto adiposo.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 209 (1966), S. 1025-1026 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The synthesis of triglycerides in rat liver depends largely on the availability of plasma free fatty acids (FFA) derived from lipolysis of triglycerides in adipose tissue6. The recent findings that drugs such as nicotinic acid7, salicylic acid8,9 and 3,5-dimethylpyrazole10 can block FFA ...
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-0778
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Summary One of the earliest biochemical effects induced by the herbicide paraquat (PQ) is damage to type II pneumocytes with consequent depletion of surfactant (Skillrud and Martin, 1984). We made a series of studies on the possible protective effect of drug ambroxol, which induces surfactant synthesis from alveolar type II cells (Post et al. 1983). The cell line A-549, exposedin vitro to PQ concentrations ranging from 0.5×10-4 to 2×10-3 M, showed a significant dose-dependent loss of viability. Ambroxol (10 mg/ml) pretreated cells were more resistant to PQ, their viability starting to decrease from a PQ concentration of 0.8×10-3 M. Membrane microviscosity was measured on the same cells. Cells treated with PQ alone showed a reduction of membrane microviscosity which was significantly counteracted by ambroxol pretreatment. The curves for membrane microviscosity of PQ and ambroxol-plus-PQ-treated cells overlapped those for cell viability, indicating that the stimulation of surfactant synthesisin vitro may be a prerequisite for counteracting some of the precocious effects of PQ. Partial protection from PQ- induced mortality was also obtainedin vivo.
    Type of Medium: Electronic Resource
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