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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 629 (1991), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of medicinal chemistry 33 (1990), S. 1892-1898 
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1750
    Keywords: Cell adhesion ; Neutrophils ; Acute lung injury ; Alveolitis ; Bronchopulmonary dysplasia ; Pulmonary function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In immature or injured lungs, impaired alveolar gas exchange forces the use of elevated levels of inhaled oxygen to maintain life. But, at high concentrations oxygen induces lung injury, edema, and bronchopulmonary dysplasia, probably by stimulating the generation of reactive oxygen radicals and subsequent neutrophil infiltration. In addition to regulating neutrophil diapedesis, intercellular adhesion molecule-1 (ICAM-1) expression is marked on inflamed alveolar epithelium, suggesting a role for ICAM-1 in oxygen-induced, neutrophil-mediated parenchymal damage. To test this, we evaluated the rat anti-mouse ICAM-1 monoclonal antibody YN 1/1.7 in 2 protocols of oxygen-induced toxicity in adult, male Balb-c mice: ≥95% O2 for 84 hr and ≥95% O2 for 60 hr followed by 48 hr at 21% (ambient) O2. YN1/1.7 treatment partially attenuated the neutrophil infiltration, lung damage (lavage lactate dehydrogenase [LDH] activity) and dysfunction (reductions in respiratory system compliance [Crs] and diffusion capacity of the lungs for carbon monoxide [DLco] in the 84 hr exposure protocol. In the milder 60 hr exposure protocol, YN1/1.7 completely blocked the oxygen-induced lung dysfunction (reductions in Crs and DLco). These results confirm the contribution of leukocytes in the pathogenesis of pulmonary oxygen toxicity and indicate that antagonism of ICAM-1 may provide a therapeutic approach to reducing hyperoxic lung injury and dysfunction.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Springer seminars in immunopathology 15 (1993), S. 75-88 
    ISSN: 1432-2196
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusion Prompted by the realization of the importance of chronic airway inflammation in allergic asthma, recent interest has focused on defining the role of adhesion glycoproteins in the development of airway inflammation and subsequent changes in airway function. Many studies in vitro and in vivo have demonstrated an increased expression of certain adhesion molecules on vascular endothelium, airway epithelium and circulating leukocytes associated with the inflammatory response to allergen. Studies with animal models of allergic asthma have shown the effectiveness of antagonists of adhesion molecules in blocking the development of airway inflammation and changes in airways function. These studies suggest that inhibitors of cellular adhesion molecules may represent a novel form of treatment directed specifically at the chronic airway inflammation characteristic of bronchial asthma.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Annals of biomedical engineering 14 (1986), S. 401-415 
    ISSN: 1573-9686
    Keywords: Linear-lumped-parameter modeling ; Parameter optimization ; Frequency dependence ; Airway wall compliance ; Lung mechanics ; Comparative respiratory mechanics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine , Technology
    Notes: Abstract Pulmonary impedance, ZL, measured from 2 to 32 Hz in anesthetized, intubated and paralyzed bonnet monkeys (Macaca radiata) was fitted to a variety of linearlumped parameter mechanical networks. Parameter values for each network were obtained by minimizing the average of the percent distance, Dr, between the computed network impedance and measured ZL at all frequencies. Measured resistance, RL, decreased from 2 to 8 Hz and increased from 8 to 32 Hz indicating that a single series resistance-inertance-compliance (RIC) network was not optimal (Dr∼19%). Networks consisting of two series RIC pathways in parallel resulted in a lower Dr (∼14%), but parameter values were difficult to interpret. Despite not modeling the decrease in RL with frequency below 8 Hz, an airway wall compliance, C aw , network in which the airways were separated into central and peripheral components resulted in an even lower Dr (∼11%). In addition, parameter values were easy to interpret, consistent among our “normal” monkeys and changed consistently and explainably with change in lung mechanics induced by decrease in lung volume. We conclude that (1) networks containing both parallel pathways and C aw are necessary to model ZL over the entire frequency range (2–32 Hz), (2) the effect of C aw is an important determinant of ZL above 8 Hz, and (3) a six-parameter C aw network with the ratio of C aw to parenchymal compliance, Cp, fixed may prove useful in interpreting changes in ZL induced by alterations in lung mechanics in monkeys.
    Type of Medium: Electronic Resource
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