This study was undertaken to evaluate the impact of chlorhexidine/silver sulphadiazine-bonded catheters on the incidence of colonisation and catheter-related sepsis in critically ill patients. Threehundred and fifty-one catheters were inserted into 228 patients during the study period, 174chlorhexidine/silver sulphadiazine-bonded catheters and 177 standard catheters. Indications for catheter removal were: death, clinical redundancy and clinical evidence of local or systemic infection. All catheter tips were sent to the microbiology laboratory for semiquantitative analysis of bacterial colony count. Seventy-one (40.2%) of the standard catheters and 47 (27.2%) of the antiseptic-bonded catheters were found to be colonised on removal (p < 0.01). Eight cases (4.7%) of catheter-related sepsis were associated with standard catheters and three cases (1.7%) with antiseptic-bonded catheters, however, this reduction was not statistically significant. Our results indicate that the use of antiseptic-bonded catheters in critically ill patients significantly reduces the incidence of bacterial colonisation.

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Server virtualization is a technology that can run multiple operating systems simultaneously on one computer. The emergence of server virtualization invites a new crime gap that is different from the challenge of finding clues and digital evidence in uncovering cases of crime. This certainly makes it difficult for investigators to make acquisitions of one of the operating systems in server virtualization without disturbing and shutting down the computer given the importance of the server. So far, acquisition techniques are generally used singly which only contains one operating system. Therefore, it is necessary to have a technique to acquire server virtualization by using the live forensics method without interrupting or shutting down other running operating systems. The use of the live forensics method to acquire server virtualization is done by applying three acquisition techniques. Three acquisition technique models are carried out by acquiring one of the operating systems that are in the virtual machine on server virtualization through the Proxmox server without turning off the other operating systems that are running. Of the three acquisition models that have been tested, it is known that there are two models of acquisition techniques that are well used and recommended based on the situation and conditions that are occurring.

Aim: P-glycoprotein (Pgp/MDR1) plays a major role in intestinal homeostasis.Decrease in Pgp function and expression has been implicated in the pathogenesis of IBD. However, inhibitory mechanisms involved in the decrease of Pgp in inflammation are not fully understood. Angiotensin II (Ang II), a peptide hormone predominantly expressed in the epithelial cells of the crypt-villus junction of the intestine, has been shown to exert pro-inflammatory effects in the gut. It is increased in IBD patients and animals with experimental colitis. Whether Ang II directly influences Pgp is not known. Methods: Pgp activity was measured as verapamil-sensitive 3 H-digoxin flux. Pgp surface expression and exocytosis were measured by cell surface biotinylation studies. Signalling pathways were elucidated by Western blot analysis and pharmacological approaches. Results: Ang II (10 nM) significantly inhibited Pgp activity at 60 minutes. Ang IImediated effects on Pgp function were receptor-mediated as the Ang II receptor 1 (ATR1) antagonist, losartan, blocked Pgp inhibition. Ang II effects on Pgp activity appeared to be mediated via PI3 kinase, p38 MAPK and Akt signalling. Ang II-mediated inhibition of Pgp activity was associated with a decrease in the surface membrane expression of Pgp protein via decreased exocytosis and was found to be dependent on the Akt pathway. Short-term treatment of Ang II (2 mg/kg b.wt., 2 hours) to mice also decreased the membrane expression of Pgp protein levels in ileum and colon. Conclusion: Our findings provide novel insights into the role of Ang II and ATR1 in decreasing Pgp expression in intestinal inflammation. K E Y W O R D SAkt, Ang II receptor 1 (ATR1), intestine, MDR1, p38 MAPK, PI3K