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Objective:To evaluate the safety of megadose meropenem as empirical treatment of nosocomial sepsis. Materials & methods:Critically ill patients diagnosed with sepsis received either high-dose (2 g every 8 h) or megadose (4 g every 8 h) meropenem as an intravenous infusion over 3 h. Results:A total of 23 patients with nosocomial sepsis were eligible and included in the megadose (n = 11) or high-dose (n = 12) group. No treatment-related adverse events were observed during a 14-day follow-up. Clinical response was also comparable between the groups. Conclusion:Megadose meropenem may be considered for empirical treatment of nosocomial sepsis without serious concern regarding its safety.

Fullerol compounds have potent antioxidant effects on biological systems. Therefore, we examined whether fullerol pretreatment potentiates the brain antioxidant defense system and decreases γ-glutamyl transpeptidase(GGT) expression during cerebral ischemia/reperfusion. Experiments were performed in three groups of rats: sham, control ischemic, and ischemic pretreatment groups. Brain ischemia was induced by 90 min of middle cerebral artery occlusion (MCAO) followed by 24 h of reperfusion. Rats received fullerol nanoparticles (10 mg/kg, intraperitoneally) 30 min before MCAO. Brain infarction, mRNA levels of GGT, glutathione content, and catalase activity were determined after 24 h reperfusion. MCAO induced extensive lesions in the right hemispheres of the control ischemic group (infarct volume 522±54 mm3) and a concomitant reduction of the glutathione content (45%) and catalase activity (56%) compared to the sham group. Fullerol in the ischemic pretreatment group significantly decreased the infarct volume (133±62 mm3) and also increased the activity of catalase by 53% compared to control. MCAO additionally increased the mRNA levels of GGT in ischemic hemispheres; however, fullerol considerably decreased the mRNA levels of this gene in the pretreatment group. The findings of the present study indicate that fullerol nanoparticles protect the ischemic brain against ischemia/reperfusion injury through potentiation of the antioxidant defense system and attenuation of GGT expression.