Developing leadership as a trainee- opportunities, barriers and potential improvements.

The General Medical Council explicitly state that doctors completing training should demonstrate capabilities in leadership and teamwork.1 However, most trainees receive little formal training in leadership. In March 2017, at the Faculty of Medical Leadership and Management (FMLM) Northern Ireland Regional Conference, a workshop on developing leadership skills as a trainee was hosted and the views of doctors in training regarding current opportunities, potential barriers and improvements were sought. In Northern Ireland presently there are a number of opportunities available for trainees to gain experience in leadership - both by learning through observation and learning through experience. These range from informal activities which do not require significant time commitment to focused, immersive leadership experiences such as ADEPT (Achieve Develop Explore Programme for Trainees)2, and the Royal College of Physicians' Chief Registrar scheme.3 Several barriers to developing leadership have been identified, including limited understanding of what constitutes leadership, a lack of senior support and little formal recognition for trainees leading teams. Time pressures, frequently rotating jobs, limited resources and difficulty upscaling can also undermine the sustainability of improvement and other leadership projects. Incorporating awareness of and training in leadership skills, as well as greater engagement with senior leaders and managers, at an early stage in training could promote understanding and encourage trainees. Formalising leadership roles within training posts may improve experience. Deaneries and Trusts can also enable leadership opportunities by facilitating study leave, raising awareness amongst supervisors, and providing career enhancing incentives for interested trainees.

Roles of genes 38, 39, and 40 in shutoff of host biosyntheses during infection of Bacillus subtilis by bacteriophage SPO1.

A nonsense mutation in SPO1 gene 40 prevented normal shutoff of both host DNA and host RNA synthesis, showing that gp40 is required for the normal occurrence of both shutoffs. A gene 39 nonsense mutation caused accelerated shutoff of both host DNA and host RNA synthesis (aided by a gene 38 nonsense mutation), showing that gp39 (aided by gp38) limits the rate at which both shutoffs occur. The 40(-) mutation suppressed the accelerative effects of the 39(-) and 38(-) mutations, showing that gp40 also plays an essential role in the accelerated shutoffs. To the best of our knowledge, proteins with the particular activities implied for gp39 and gp40 have not been identified in any other bacteriophage. SPO1 has at least three different mechanisms that have the effect of delaying the shutoff of host DNA and RNA synthesis.

Hepatotoxicity and gastrointestinal intolerance when healthy volunteers taking rifampin add twice-daily atazanavir and ritonavir.

BACKGROUND: Rifampin is the cornerstone of antituberculosis therapy, but induction of hepatic cytochrome P4503A by rifampin markedly lowers HIV protease inhibitor plasma concentrations. METHODS: This phase 1, open-label, one-arm study was designed to assess pharmacokinetic interactions and safety of atazanavir, ritonavir, and rifampin among 14 evaluable HIV-seronegative volunteers. The study included 3 sequential periods of study drug dosing, with plasma sampling for pharmacokinetic analyses to occur on the last day of each period. During period 1, participants received rifampin 600 mg every 24 hours for 8 days. During period 2, participants continued rifampin 600 mg every 24 hours, and added atazanavir 300 mg and ritonavir 100 mg every 12 hours, to continue for at least 11 days. During period 3, atazanavir was to be increased to 400 mg every 12 hours. RESULTS: Upon adding atazanavir and ritonavir, the first 3 subjects developed vomiting and transaminase elevations resulting in study drug discontinuation. The study was therefore terminated. CONCLUSIONS: Coadministration of rifampin with HIV protease inhibitors may not be a viable treatment option if rifampin administration precedes protease inhibitor initiation. Future studies, which explore concomitant HIV protease inhibitors with rifampin must carefully consider the sequence in which drugs are initiated.