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Nitric oxide response

Although reaction (xliii) appears to be the major reaction between H atoms and nitrous oxide, this does not exclude the occurrence of the alternative reaction (xliv). Indeed reaction (xliv) has been specifically suggested to explain (a) the formation of the nitric oxide responsible for the sensitizing effect of N2O on H2 + O2 explosions [268] (cf. Sect. 8.3), and (b) the formation of nitric oxide in H2+ N2O flames at 1500—2000 K [293] and shocked gases at 1900—2800 K [294]. More recent investigations of the thermal H2+N2O reaction have also shown that the mechanism is more complex than that suggested by Melville [287, 288]. [Pg.160]

Martin, L.P., Pham, A.Q. and Glass, R.S. (2003) Effect of Cr2O3 electrode morphology on the nitric oxide response of a stabilized zirconia sensor. Sens. Actuators B, 96, 53-60. [Pg.482]

Klein-Nulend, J. et al. Nitric oxide response to shear stress by human bone ceU cultures is endothelial nitric oxide synthase dependent. Biochem. Biophys. Res. Commun., 250,108,1998. [Pg.714]

Btlsch A, Pohhnarm A, Friedrich B, Cramm R. 2004. A DNA region recognized by the nitric oxide-responsive transcriptional activator NorR is conserved in beta- and gamma-proteobacteria. J Bacterial 186 7980-7987. [Pg.393]

Ridnour, L.A., Thomas, D.D., Donzelli, S., Espey, M.G., Roberts, D.D., Wink, D.A., and Isenberg, J.S. (2006). The bipha.sic nature of nitric oxide responses in tumor biology. Antioxid Redox Signals, 1329-1337. [Pg.129]

Wang, S., Wang, W., Wesley, R.A., and Danner, R.L. (1999). A Spl binding site of the tumor necrosis factor alpha promoter functions as a nitric oxide response element. J. Biol. Chem. 274, 33190-33193. [Pg.458]

Other possible modes of action may centre on stimulation of T cells (this occurred with the live aroA mutant of A. salmonicida Marsden et al., 1996), which introduces the role of cellular and innate rather than humoral immunity as the mode of action. For this, examples include A. hydrophila LPS (Baba et al., 1988) and E. tarda ECPs (Lee et al., 2010). Of course, there could be involvement of humoral, cell-mediated and innate immune parameters as stated for the i.p. administration of a live auxotrophic aroA mutant of A. hydrophila with effectiveness against furunculosis in rainbow trout (Vivas et al, 2004). Other possibilities include the evidence that one commercial formalized whole cell V. anguillarum vaccine induces Mx gene (these are inducible by Type I interferons and have a role in antiviral activity) expression in Atlantic salmon after administration intraperitoneally (Acosta et al., 2004). In another example, vaccination with P. damselae subsp. piscicida cells were found to enhance the nitric oxide response, i.e. the production of reactive nitrogen intermediates with their antimicrobial activities, to infection with the pathogen, and is correlated with the level of protection (Acosta et al., 2005). There was inhibition of F columnare adhesion to the skin of immersion vaccinated eel (Mano et al., 1996). Finally, mention will be made of a possible mechanism of protection of V. anguillarum vaccines that may well involve the inhibition of bacterial attachment by unknown factors in the skin mucus (Kawai and Kusuda, 1995). [Pg.233]

Influence of vaccination on the nitric oxide response of gilthead seabream following infection with Photobacterium damselae subsp. piscicida. Fish Shellfish Immunology 18,31-38. [Pg.234]

Apelins and the Apelin Receptor. Figure 3 Scheme illustrating the hypothesised mechanisms of control of human (a) vasculartone and (b) cardiac contractility by apelin peptides ( ). In the vasculature, apelins (released via the small vesicles of the constitutive pathway) may act directly to activate apelin receptors on the underlying smooth muscle to produce vasoconstriction. This response may be modified by apelin peptides feeding back onto apelin receptors on endothelial cells to stimulate the release of dilators, such as nitric oxide. In heart, apelin peptides, released from endocardial endothelial cells, activate apelin receptors on cardiomyocytes to elicit positive inotropic actions. [Pg.205]

The human histamine Hi-receptor is a 487 amino acid protein that is widely distributed within the body. Histamine potently stimulates smooth muscle contraction via Hi-receptors in blood vessels, airways and in the gastrointestinal tract. In vascular endothelial cells, Hi-receptor activation increases vascular permeability and the synthesis and release of prostacyclin, plateletactivating factor, Von Willebrand factor and nitric oxide thus causing inflammation and the characteristic wheal response observed in the skin. Circulating histamine in the bloodstream (from, e.g. exposure to antigens or allergens) can, via the Hi-receptor, release sufficient nitric oxide from endothelial cells to cause a profound vasodilatation and drop in blood pressure (septic and anaphylactic shock). Activation of... [Pg.589]

Kudo FA, Warycha B, Juran PJ, Asada H, Teso D, Aziz F (2005) Differential responsiveness of early- and late-passage endothehal cells to shear stress. Am J Surg 190(5) 763-769 Lee RH, Efron D, Tantry U, Barbul A (2001) Nitric oxide in the healing wound a time-course study. J Surg Res 101(1) 104-108... [Pg.349]


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See also in sourсe #XX -- [ Pg.26 , Pg.937 , Pg.938 , Pg.939 , Pg.940 , Pg.941 , Pg.942 , Pg.943 , Pg.944 , Pg.945 , Pg.946 , Pg.947 , Pg.948 ]

See also in sourсe #XX -- [ Pg.921 , Pg.922 ]




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