The impact of clinical simulation on the development of advanced practice skills.

This article considers the findings of a qualitative research study into the impact of simulation on the development of advanced clinical practitioners' skills and knowledge. STUDY AIM: To explore simulated learning through the eyes of trainee and trained advanced clinical practitioners (ACPs) and consider its potential in supporting their development. METHOD: This qualitative research study explored the experiences of trained and trainee ACP volunteers undertaking a structured simulated event provided by a local acute hospital trust simulation team. A questionnaire (n=10) and a focus group (n=4) acted as the data gathering tools. RESULTS: Although simulation can be daunting for the participants, the overwhelming outcome was positive. Participants stated that they gained confidence and suggested that simulation offered a safe place to practise the challenging scenarios that occur in the clinical environment. Additionally, they emphasised that simulation provided a place to network and receive constructive feedback that was non-judgemental, and which helped them to develop clinical knowledge and appreciate their limitations. CONCLUSION: Simulation is a valuable addition to the education and development of ACPs. It should be considered for inclusion within the educational curriculum as a supplement to theoretical knowledge and to the structured clinical supervision provided within the clinical environment.

The antimalarial drug quinine interferes with serotonin biosynthesis and action.

The major antimalarial drug quinine perturbs uptake of the essential amino acid tryptophan, and patients with low plasma tryptophan are predisposed to adverse quinine reactions; symptoms of which are similar to indications of tryptophan depletion. As tryptophan is a precursor of the neurotransmitter serotonin (5-HT), here we test the hypothesis that quinine disrupts serotonin function. Quinine inhibited serotonin-induced proliferation of yeast as well as human (SHSY5Y) cells. One possible cause of this effect is through inhibition of 5-HT receptor activation by quinine, as we observed here. Furthermore, cells exhibited marked decreases in serotonin production during incubation with quinine. By assaying activity and kinetics of the rate-limiting enzyme for serotonin biosynthesis, tryptophan hydroxylase (TPH2), we showed that quinine competitively inhibits TPH2 in the presence of the substrate tryptophan. The study shows that quinine disrupts both serotonin biosynthesis and function, giving important new insight to the action of quinine on mammalian cells.