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  • 1
    Electronic Resource
    Electronic Resource
    Methanol and ethanol oxidation by chromium(VI) in aqueous perchloric acid (1993)
    Springer
    Transition metal chemistry 18 (1993), S. 329-334 
    Details
    ISSN: 1572-901X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Summary Oxidation of short-chain alcohols (MeOH and EtOH) by CrVI in concentrated aqueous HClO4 does not fit pseudo-first order rate equations, but results can be expressed in a two-exponential equation. A reaction mechanism based upon a chromate ester intermediate in equilibrium with the protonated alcohol and the chromic acid, suitable for a longer chain alcohol, does not account for kinetic results. A new mechanism is considered involving an intermediate reaction between chromic and perchloric acids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00207958
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  • 2
    Electronic Resource
    Electronic Resource
    Involvement of calcium in the stimulation of phosphatidylcholine secretion in primary cultures of rat type II pneumocytes by Escherichia coli lipopolysaccharide (2000)
    Springer
    Molecular and cellular biochemistry 205 (2000), S. 39-44 
    Details
    ISSN: 1573-4919
    Keywords: pulmonary surfactant ; endotoxic shock ; lipopolysaccharide ; type II pneumocytes ; phosphatidylcholine secretion ; intracellular Ca2+
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The purpose of this study was to evaluate the mechanism by which Escherichia coli lipopolysaccharide stimulates the secretion of phosphatidylcholine in primary cultures of rat type II pneumocytes. The stimulatory effect of lipopolysaccharide on phosphatidylcholine secretion was additive to those of terbutaline and TPA (protein kinase A and C activators respectively) and this effect was not suppressed by inhibitors of both protein kinases. On the other hand, lipopolysaccharide did not modify the increase on phosphatidylcholine secretion induced by the endoplasmic reticulum Ca2+-ATPase inhibitor thapsigargin, and enhanced slightly the calcium-ionophore A23187 stimulated phosphatidylcholine secretion. In addition, the stimulatory effect of lipopolysaccharide was suppressed by BAPTA, an intracellular Ca2+ chelator, and KN-62, a specific inhibitor of Ca2+-calmodulin-dependent protein kinase. These results, together with the lipopolysaccharide-mediated increase in the cytosolic [Ca2+], suggest that stimulation of phosphatidylcholine secretion by lipopolysaccharide in type II pneumocytes occurs by a calcium-dependent transduction mechanism via Ca2+-calmodulin-dependent protein kinase activation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007040708579
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  • 3
    Electronic Resource
    Electronic Resource
    The relationship between dietary fat intake and risk of colorectal cancer: evidence from the combined analysis of 13 case-control studies (1997)
    Springer
    Cancer causes & control 8 (1997), S. 215-228 
    Details
    ISSN: 1573-7225
    Keywords: Case-control studies ; colorectal neoplasms ; dietary fat ; energy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The objective of this study was to examine the effects of the intakeof dietary fat upon colorectal cancer risk in a combined analysis of datafrom 13 case-control studies previously conducted in populations withdiffering colorectal cancer rates and dietary practices. Original datarecords for 5,287 cases of colorectal cancer and 10,470 controls werecombined. Logistic regression analysis was used to estimate odds ratios (OR)for intakes of total energy, total fat and its components, and cholesterol.Positive associations with energy intake were observed for 11 of the 13studies. However, there was little, if any, evidence of anyenergy-independent effect of either total fat with ORs of 1.00, 0.95, 1.01,1.02, and 0.92 for quintiles of residuals of total fat intake (P trend =0.67) or for saturated fat with ORs of 1.00, 1.08, 1.06, 1.21, and 1.06 (Ptrend = 0.39). The analysis suggests that, among these case-control studies,there is no energy-independent association between dietary fat intake andrisk of colorectal cancer. It also suggests that simple substitution of fatby other sources of calories is unlikely to reduce meaningfully the risk ofcolorectal cancer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018476414781
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  • 4
    Electronic Resource
    Electronic Resource
    Impaired phosphatidylcholine biosynthesis and ascorbic acid depletion in lung during lipopolysaccharide-induced endotoxaemia in guinea pigs (1997)
    Springer
    Molecular and cellular biochemistry 175 (1997), S. 117-123 
    Details
    ISSN: 1573-4919
    Keywords: endotoxic shock ; lipopolysaccharide ; guinea pig ; lung ; phosphatidylcholine ; ascorbic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Injection of guinea pigs with a single dose of Escherichia coli lipopolysaccharide (3.2 mg/100 g) induces a reversible endotoxic shock that was evaluated by measuring plasma glucose levels and aspartate aminotransferase activity at 24 h after lipopolysaccharide injection. The hypoglycaemia and the increase in plasma aminotransferase activity observed, correlated with the alterations found during the recovery phase of endotoxic shock. When lipid peroxidation and some antioxidant systems were measured in lungs from treated animals, we only found differences in ascorbic acid content, that was decreased by 50%. Lipopolysaccharide treatment results in a depression of pulmonary phosphatidylcholine synthesis, that correlates with the surfactant deficiencies associated with respiratory illnesses in septic shock. Guinea pigs fed on a diet with a low content in ascorbic acid were more sensitive to endotoxin. In these animals we found no detectable levels of ascorbic acid in lung, whereas both vi tamin E lung levels and pulmonary phosphatidylcholine synthesis were significantly decreased. Our results point out the significance of ascorbic acid in the protection against oxidative lung injury associated to endotoxaemia, and validate our shock model for further studies on the mechanisms of this pathological condition. (Mol Cell Biochem 175: 117–123, 1997)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006883628365
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  • 5
    Electronic Resource
    Electronic Resource
    The inflammatory cytokines tumor necrosis factor α and interleukin-1β stimulate phosphatidylcholine secretion in primary cultures of rat type II pneumocytes (1998)
    Springer
    Molecular and cellular biochemistry 189 (1998), S. 169-176 
    Details
    ISSN: 1573-4919
    Keywords: pulmonary surfactant ; lipopolysaccharide ; TNFα ; IL-1β ; TypeII pneumocytes ; phosphatidycholine secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Tumor necrosis factor α and interleukin-1β increase surfactant secretion in type II pneumocytes in a time- and dose-dependent manner. This stimulatory effect was additive to that of lipopolysaccharide, suggesting that cytokines and lipopolysaccharide may exert their actions through different signal transduction pathways. Tumor necrosis factor α and interleukin-1β did not modify the increase on phosphatidylcholine secretion induced by the direct protein kinase C activator tetradecanoylphorbol 13-acetate, whereas this effect was inhibited by the protein kinase C inhibitors bisindolylmaleimide (2 × 10-6M) and 1-(5-isoquinolinylsulphonyl)-2-methyl piperazone (10-4M). In addition, the stimulatory effect of tumor necrosis factor α and interleukin-1β was not suppressed by the intracellular Ca2+ chelator BAPTA (5 × 10-6M) or by KN-62 (3 × 10-5M), a specific inhibitor of Ca2+-calmodulin-dependent protein kinase. These results suggest that tumor necrosis factor α or interleukin-1β stimulate phosphatidylcholine secretion via protein kinase C activation in a Ca2+ -independent manner.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006997731607
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    Paper (German National Licenses)
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