Second, 5 different types of DES were used in the three trials included in the present analysis. We therefore analyzed differences using mixed models accounting for different trials as well as treatment arms. Moreover, the use of different types of DES afford a certain generalizability of our findings to DES as a class treatment effect. Third, only 63 patients had a GFR,30 ml/min at baseline and patients requiring hemodialysis were not captured in the pooled trials. Evaluation of the safety and effectiveness of DES in patients with severely impaired renal function and in those requiring hemodialysis will certainly prompt additional investigations. Fourth, bleeding events were not captured in the three pooled trials. Therefore, we were not able to compared bleeding risks between groups. Finally, the angiographic follow-up was not available for all included patients. Nevertheless, the consistency of angiographic surveillance findings and the correlation with clinical outcomes support our finding of equivalent effectiveness of DES in patients with coronary artery disease undergoing PCI regardless of renal function. Gram negative nosocomial pathogen Pseudomonas aeruginosa causes a variety of infections including spontaneous bacterial peritonitis pyogenic liver abscess, sepsis and septic shock. Endotoxin, which is a hydrophobic glycolipid, is known to play a very imperative role in pathogenesis of P. aeruginosa XAV939 mediated infections. It is well recognized that cell free endotoxin is significantly more biologically functional than cell bound endotoxin and antibiotics, particularly those that act as inhibitors of cell wall biosynthesis, induce enormous amount of endotoxin release during treatment. Plenty of experimental evidences from in vitro, in vivo and ex vivo models have advocated that antibiotics vary in their ability to trigger endotoxin release from gramnegative microbes. Further, ex vivo evaluation of whole mouse blood has established that there is a correlation between amount of endotoxin release following antibiotic exposure and pro-inflammatory cytokine production. Though liver is known to detoxify endotoxin but at the same time it also responds energetically to endotoxin leading to endotoxin induced inflammations. In liver, LBP binds to endotoxin and activates CD14, toll-like receptor 4 and MD2 surface receptor complex of macrophages, monocytes, hepatocytes and kupffer cells resulting in potent inflammatory response. Endotoxin binds with TLR4 receptor which is highly expressed in cells that respond to endotoxin, such as macrophages, monocytes, hepatocytes and kupffer cells and induces expression of inflammatory genes through TLR4/NF-kB signaling pathway. NF-kB family consists of five structurally related proteins known as Rel/NF-kB proteins; p50, p52, RelA, RelB, and c-Rel. Two signaling pathways are involved in the activation of NF-kB family. Canonical pathway and non-canonical pathway. Canonical signaling pathway includes toll-like receptor super family which is helpful in recruitment of adaptor molecules such as TRAF to cytoplasmic domain of the receptor. The canonical pathway induction involves RelA, RelB, c-Rel and p50 proteins to activate NF-kB.