No abstract

Many different methods have been used to study the incidence of prescribing errors in hospital inpatients. The objectives of this review were to outline the methods used, highlight their strengths and limitations, and summarise the incidence of prescribing errors reported. Methods used may be retrospective or prospective and based on process or on outcome. Reported prescribing error rates vary widely, ranging from 0.3% to 39.1% of medication orders written and from 1% to 100% of hospital admissions. Unfortunately, there is no standard denominator for use when expressing prescribing error rates. It could be argued that the most meaningful is the number of medication orders written; however, it is also helpful to consider the number of medication orders written per patient stay in order to understand the risk that a given prescribing error rate poses to an individual patient. Because of wide variation in the definitions and methods used, it is difficult to make comparisons between different studies. Each method for identifying prescribing errors has advantages and disadvantages. Process-based studies potentially allow all errors to be identified, giving more scope for the identification of trends and learning opportunities, and it may be easier to collect sufficient data to show statistically significant changes in prescribing error rates following interventions to reduce them. However, studies based on process may be criticised for focusing on many minor errors that are very unlikely to have resulted in patient harm. Focusing instead on harm, as in outcome-based studies, allows efforts to reduce errors to be targeted on those areas that are likely to result in the highest impact. Therefore, the most appropriate method depends on the study's aims. However, using a combination of methods is likely to be the most useful approach if comprehensive data are required.

The ability to precisely monitor and manipulate neural circuits is essential to understand the brain. Advancements over the last decade in optical techniques such as calcium imaging and optogenetics have empowered researchers to gain insight into brain function by systematically manipulating or monitoring defined neural circuits. Combining these cutting-edge techniques enables a more direct mechanism for ascribing neural dynamics to behavior. Here, we developed a miniaturized integrated microscope that allows for simultaneous optogenetic manipulation and cellular-resolution calcium imaging within the same field of view in freely behaving mice. The integrated microscope has two LEDs, one filtered with a 435–460 nm excitation filter for imaging green calcium indicators, and a second LED filtered with a 590–650 nm excitation filter for optogenetic modulation of red-shifted opsins. We developed and tested this technology to minimize biological and optical crosstalk. We observed insignificant amounts of biological and optical crosstalk with regards to the optogenetic LED affecting calcium imaging. We observed some amounts of residual crosstalk of the imaging light on optogenetic manipulation. Despite residual crosstalk, we have demonstrated the utility of this technology by probing the causal relationship between basolateral amygdala (BLA) -to- nucleus accumbens (NAc) circuit function, behavior, and network dynamics. Using this integrated microscope we were able to observe both a significant behavioral and cellular calcium response of the optogenetic modulation on the BLA-to-NAc circuit. This integrated strategy will allow for routine investigation of the causality of circuit manipulation on cellular-resolution network dynamics and behavior.

Although we identified some ADEs using the trigger tool, more work is needed to further refine the trigger tool to reduce the false positives and increase sensitivity. To comprehensively identify preventable ADEs, retrospective health record review remains the gold standard and we found no efficiency gain in using the trigger tool.

CVD is a major cause of mortality and morbidity in the Western world. In recent years its importance has expanded internationally and it is believed that by 2020 it will be the biggest cause of mortality in the world, emphasising the importance to prevent or minimise this increase. A beneficial role for vitamins in CVD has long been explored but the data are still inconsistent. While being supported by observational studies, randomised controlled trials have not yet supported a role for vitamins in primary or secondary prevention of CVD and have in some cases even indicated increased mortality in those with pre-existing late-stage atherosclerosis. The superiority of combination therapy over single supplementation has been suggested but this has not been confirmed in trials. Studies have indicated that β-carotene mediates pro-oxidant effects and it has been suggested that its negative effects may diminish the beneficial effects mediated by the other vitamins in the supplementation cocktail. The trials that used a combination of vitamins that include β-carotene have been disappointing. However, vitamin E and vitamin C have in combination shown long-term anti-atherogenic effects but their combined effect on clinical endpoints has been inconsistent. Studies also suggest that vitamins would be beneficial to individuals who are antioxidant-deficient or exposed to increased levels of oxidative stress, for example, smokers, diabetics and elderly patients, emphasising the importance of subgroup targeting. Through defining the right population group and the optimal vitamin combination we could potentially find a future role for vitamins in CVD.