BACKGROUNDEmergency color codes were developed to alert healthcare personnel in a hospital to critical situations. They are often developed independently by each hospital, leading to variability. This could be a source of confusion to healthcare personnel, who move frequently between hospitals and may work at multiple hospitals. This study evaluated the variability of emergency codes for different critical events in hospitals in Riyadh.METHODSA prospective, cross-sectional survey was carried out on a representative sample of hospitals. Twenty-four of 28 hospitals took part in the study. Semi-structured questionnaires were completed by the Quality/Safety Department of each hospital, on general hospital characteristics, emergency department characteristics, code-response mock-up, code determination, emergency codes used and code meanings.RESULTSThirty-four different codes were used across hospitals. The codes used most variably were yellow (10 meanings), orange, black, green (7 meanings each), and gray (5 meanings), while the most consistently used code was ‘Code Red’ for ‘Fire’ in 75% of hospitals. Another source of variability was the use of non-color codes, representing 7.7% of total codes.CONCLUSIONSThere is large variability in the type and meaning of emergency codes between hospitals in Riyadh City, reflecting a lack of standardization. Hospitals use color and non-color emergency codes, which could cause confusion to responders and mitigate the effectiveness and speed of response in critical events.

ObjectiveElevated Reactive Oxygen Species (ROS) in Endothelial Cells (EC's) have been implicated in the pathogenesis of cardiovascular diseases, and much research has gone into elucidating the mechanisms through which oxidative stress leads to these diseases. Research in the last decade, however, has uncovered the central role lower levels of ROS play in physiological intracellular signaling pathways, such as those stimulated by Vascular Endothelial Growth Factor (VEGF) and Tumour Necrosis Factor‐α (TNF‐α) in EC's. Our objective in this study was to determine the effect of a lack of ROS in EC's on the intracellular signaling pathways stimulated by VEGF and TNF‐α.MethodsThe activity of these pathways can be measured by the expression of key downstream proteins that are common to these two pathways such as Akt, ERK‐1/2, IKKα/B, AMPK, eNOS, mTOR and FOXO1. To investigate these pathways in vitro, Bovine Endothelial Aortic Cells (BAEC's) were treated with ROS inhibitors (NAC, DPI) and then exposed to VEGF or TNF‐α to stimulate their respective pathways. Protein was then extracted and transferred to a membrane by Western Blotting then visualized by immunoflourescence.ResultsWestern blots demonstrated that reduction of ROS levels by NAC inhibited VEGF‐induced Akt phosphorylation but not phosphorylation of ERK1/2 in BAEC. The findings of TNF‐induced signaling activation were not conclusive.ConclusionWhereas VEGF‐mediated activation of PI3K‐Akt activation requires ROS, ERK1/2 activation is independent of ROS in ECs.This research was funded by National Institutes of Health (NIH) and American Heart Association (AHA) grants.