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Previous studies demonstrated an enhancing effect of granulocyte-macrophage colony-stimulating-factor (GM-CSF) on natural cytotoxicity. It was the aim of this study to investigate if CD56+ natural-killer (NK) cells are responsible for the increased natural cytotoxicity after GM-CSF treatment. NK-cells were incubated with or without GM-CSF and Interferon-α (IFN-α) at various concentrations. NK-activity was determined by their ability to lyse NK-sensitive tumor cells (K562) and by cell surface expression of activation markers (CD25 and CD69). In our experimental setting incubation of CD56+ NK-cells with GM-CSF did not significantly alter NK-cell mediated cytotoxicity or the expression of activation markers. In contrast, pre-treatment with IFN-α, a well known stimulant of NK-activity enhanced cytotoxicity by 69.2%±13.2%, P<0.05, effector/target cell ratio (E/T) 10:1 and by 43.3%±17.3%, P<0.05, E/T 20:1 and increased the expression of CD69 and CD25. Our results suggest that GM-CSF treatment alone cannot enhance natural cytotoxicity mediated by CD56+ NK-cells in vitro. [Copyright &y& Elsevier]

Background: Cerebral microemboli (ME) are frequently generated during orthopaedic surgery and may impair cerebral integrity. However, the nature of cerebral ME, being either of solid or gaseous origin, is poorly investigated. Our primary aim was to determine both the frequency and nature of cerebral ME in generally anaesthetised patients undergoing major orthopaedic surgery.Methods: Fifty patients (hip/knee/shoulder prosthesis, spine surgery) were enrolled. Cerebral ME and cerebral blood flow velocity (CBFV) were determined in both middle cerebral arteries for 15 min preoperatively and postoperatively, using transcranial Doppler ultrasound. Cerebral tissue oxygen index, determined by near-infrared spectroscopy, was further examined. Statistical analysis was carried out using the Wilcoxon matched-pairs signed-ranks test (median (25 th ; 75 th percentile), P  < 0.05).Results: Overall the frequency of postoperative cerebral ME rose to 600% of preoperative values. Primarily gaseous ME occurred preoperatively and postoperatively [19 (6; 63) vs 116 (24; 373), P  < 0.001], while the number of solid ME was negligibly small [1 (0; 2) vs 2 (0; 6), P  < 0.001]. CBFV and cerebral tissue oxygen index remained unaltered bilaterally before and after surgery.Conclusions: Our findings indicate that cerebral ME considerably increase after major orthopaedic surgery under general anaesthesia. The predominant accumulation of gaseous ME and their preoperative occurrence, suggest that the general anaesthesia and individual patient factors may contribute to the embolic load in addition to orthopaedic surgery.Clinical trial registration: . NCT02340416. [ABSTRACT FROM AUTHOR]