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  • Blackwell Publishing Ltd  (2)
  • Wiley-Blackwell  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Business strategy review 15 (2004), S. 0 
    ISSN: 1467-8616
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Economics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Decision sciences 1 (1970), S. 0 
    ISSN: 1540-5915
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Economics
    Notes: The central problem area in marketing may be conceived as the analysis and satisfaction of the consumer-buyer in order to stimulate demand. In its most fundamental form, therefore, marketing is necessarily concerned with describing, explaining, and predicting the behavior of men as it pertains to the performance of marketing activities, including consumption. That is, marketing is necessarily concerned with the development of a general theory and within it, a theory of consumer behavior.In this article, the authors propose one possible foundation for a theory of consumer behavior. Towards this end, the nature of theory, the primary requirements of developing consumer theory and some of the problems presently encountered in meeting these requirements, are all considered. A theoretical approach which holds promise for overcoming these problems, relevant to theory-development requirements, is then presented.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 138 (1989), S. 165-174 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: A single infusion of Escherichia coli endotoxin into sheep results in structural evidence of pulmonary endothelial injury, increases in both prostacyclin and prostaglandin E2 (PGE2) in lung lymph, and an increase in pulmonary micro-vascular permeability. Endotoxin-induced lung endothelial damage can also be induced in vitro, but to date these studies have utilized endothelium from large pulmonary vessels. In the present study, we have grown endothelial cells from peripheral lung vessels of cows and sheep and exposed these microvascular endothelial cells to endotoxin. Controls included lung microvascular endothelium without endotoxin and endothelial cells from bovine and sheep main pulmonary artery with and without addition of endotoxin. We found that endotoxin caused significant increases in release of prostacyclin and PGE2 from both bovine and sheep lung microvascular and pulmonary artery endothelium. Normal bovine and sheep pulmonary artery and bovine lung microvascular endothelium released greater levels of prostacyclin than PGE2 (ng/ng); release of PGE2 from the microvascular cells was greater than from the pulmonary artery endothelium in both species. Exposure of endothelial cells from cow and sheep main pulmonary artery to endotoxin results in endothelial cell retraction and pyknosis, a loss of barrier function, increased release of prostacyclin and PGE2 and eventual cell lysis. In lung microvascular cells, the increases in prostanoids were accompanied by changes in cell shape but occurred in the absence of either detectable alterations in barrier function or cytolysis. Thus, while endotoxin causes alterations to endothelial cells from both large and small pulmonary vessels, the effects are not identical suggesting site specific phenotypic expression of endothelial cells even within a single vessel. To determine whether the response of either the large or small pulmonary vessel endothelial cells in culture mimics most closely the in vivo response of the lung to endotoxin requires further study.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
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