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Surfactant recruitment

Surfaetant dysfimction has been demonstrated in a guinea pig model of allergic asthma (236), and in this model the airway narrowing can be alleviated by surfactant inhalation (237). Surfactant protein A is deficient in the bronchoal-veolar fluid of some asthmatics (238). Recently, Kurashima et al. (239) have demonstrated that, during the early phase of an asthmatic attack, decreases in the surface activity of sputum from asthmatic patients were ameliorated during the late phase, possibly as a result of surfactant recruitment. Pilot studies have shown that surfactant inhalation may alleviate the symptoms of asthma (240). [Pg.561]

Comparative mechanistic studies on the microemulsion polymerization of styrene and methyl methacrylate were carried out by several groups [67,73-77,79,81,83,90-93,128]. The results could be coherently interpreted in terms of the relative monomer solubilities in water. In the case of styrene, which has a very low solubility in water (0.031%), it was postulated that initiation takes place in the microemulsion droplets. The polymer particles grow by recruiting monomer and surfactant from uninitiated droplets. Homogeneous nucleation in styrene systems may be relatively insignificant due to the large number of microemulsion droplets, which will capture most of the radicals generated in the aqueous phase before they reach a critical size for precipitation. [Pg.692]

C5a is chemotacdc, recruiting neutrophils and macrophages to the site of injury [174]. Here, it stimulates the release of lysosomal enzymes, leukotrienes, and reactive oxygen species by maorophages. Currently, little is known about the involvement of the peptide mediators in surfactant-induced irritation. [Pg.459]

Subjects with skin sensitive to surfactants tend to develop skin reactions in their presence more readily than the average population. Many products have been developed for those consumers. When such products are tested on human volimteers, test subjects are recruited from the sensitive-skin population according to criteria defined in the literature (e.g.. Refs. 142 and 143). [Pg.501]

PEEP is defined as an elevation of transpulmonary pressures at the end of expiration (17). It prevents alveoli from de-recruiting during expiration, which is beneficial, as recruited alveoli improve V/Q matching and gas exchange (12-14), patent alveoli are not exposed to the risk of injury from the stress of repeated opening and closing (17,18), and recruited alveoli prevent surfactant breakdown, thus improving CL (19). [Pg.16]


See other pages where Surfactant recruitment is mentioned: [Pg.207]    [Pg.310]    [Pg.127]    [Pg.468]    [Pg.15]    [Pg.180]    [Pg.110]    [Pg.273]    [Pg.196]    [Pg.307]    [Pg.307]    [Pg.308]    [Pg.269]    [Pg.81]    [Pg.434]   
See also in sourсe #XX -- [ Pg.561 ]




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Recruitment

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