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Nurses are responsible for medication administration, and, as with many other nursing interventions, some risk is involved. If an error occurs, a patient may suffer harm or injury, which may lead to a permanent disability or a fatality. To ensure safe drug administration, nurses are encouraged to follow the five rights ('R's; patient, drug, route, time and dose) of medication administration to prevent errors in administration. The five 'R's do not consider all causes of drug errors; instead, they focus on medication administration at the bedside so they relate only to this stage of a drug prescription. A drug's journey is more than what happens at the bedside; therefore, the reduction of errors requires more than just the five 'R's. This article proposes a multi-professional, evidence-based approach to medicines management, which all clinicians can work towards, together. Clinicians can achieve this approach by considering the National Patients Safety Agency's definition of a medication error and the values set out by the National Prescribing Centre. The approach utilizes 10 'R's, which provide a benchmark for good practice. The 10 'Rs' advocate the need for the knowledge of the causes of drug errors, how to implement strategies to reduce drug errors, how to ensure safe practice throughout the medication journey, from chemical preparation, to monitoring outcomes, to response.

Background Atopic dermatitis (AD) is a common, complex, and highly heritable inflammatory skin disease. Genome-wide association studies offer opportunities to identify molecular targets for drug development. A risk locus on chromosome 11q13.5 lies between 2 candidate genes, EMSY and LRRC32 (leucine-rich repeat-containing 32) but the functional mechanisms affecting risk of AD remain unclear. Objectives We sought to apply a combination of genomic and molecular analytic techniques to investigate which genes are responsible for genetic risk at this locus and to define mechanisms contributing to atopic skin disease. Methods We used interrogation of available genomic and chromosome conformation data in keratinocytes, small interfering RNA (siRNA)–mediated knockdown in skin organotypic culture and functional assessment of barrier parameters, mass spectrometric global proteomic analysis and quantitative lipid analysis, electron microscopy of organotypic skin, and immunohistochemistry of human skin samples. Results Genomic data indicate active promoters in the genome-wide association study locus and upstream of EMSY ; EMSY , LRRC32 , and intergenic variants all appear to be within a single topologically associating domain . siRNA-knockdown of EMSY in organotypic culture leads to enhanced development of barrier function, reflecting increased expression of structural and functional proteins, including filaggrin and filaggrin-2, as well as long-chain ceramides. Conversely, overexpression of EMSY in keratinocytes leads to a reduction in markers of barrier formation. Skin biopsy samples from patients with AD show greater EMSY staining in the nucleus, which is consistent with an increased functional effect of this transcriptional control protein. Conclusion Our findings demonstrate an important role for EMSY in transcriptional regulation and skin barrier formation, supporting EMSY inhibition as a therapeutic approach.

CB11 immunohistochemistry accurately predicts HER2 amplification status and can be reliably carried out on core biopsy specimens of breast carcinoma.