“…In addition, however studies in experimental and clinical models have clearly demonstrated other activities on pro-infl ammatory mediators involved in the actions of NSAIDs in providing relief from infl ammation and pain (Kitchen et al, 1985;Hunneyball et al, 1989;Rainsford, 1996;Celotti and Laufer, 2001;Tarnawski and Jones, 2003;Rainsford, 2004;). Among these mechanisms are the inhibition of leucocyte accumulation at infl amed sites, activation and expression of cell surface receptors, of angiogenesis, cell apoptosis, reactive oxygen species (ROS, or oxyradicals and nitric oxide) and their actions, and the regulation of non-prostanoid lipid mediators (Kitchen et al, 1985;Hunneyball et al, 1989;Rainsford, 1996;Tarnawski and Jones. 2003;Rainsford 2004aRainsford , 2004bCelotti and Laufer, 2001;Serhan, 2004) Aside from individual variations in pharmacological effects NSAIDs also differ substantially in the pharmacokinetic, pharmacological, pharmacodynamic and in their clinical profi les (Hart and Huskisson, 1984;Brogden, 1986;Bannwarth et al, 1989;Levy and Smith, 1989;Netter et al, 1993;Evans, 1996;Hayball, 1996;Rainsford, 1996;Lefkowith 1999;Heyneman et al, 2000;Verbeeck 1990; Celotti and Laufer, 2001;Day 2001;Landoni snd Scoraci, 2001;Bijlsma 2002;Tarnawski and Jones, 2003;Rainsford et al, 2005aRainsford et al, , 2005bHuntjens et al, 2005).…”