Teams are an integral component of quality improvement efforts in healthcare organizations. Quality improvement teams may involve persons either from the same or different disciplines. In either case, the selection of team members may be critical to the team's success. However, there is little research to guide selection of team members for quality improvement teams. In this paper, we use tools from social network analysis (SNA) to derive principles for the design of effective clinical quality improvement teams and explore the implementation of these principles using social network data collected from the inpatient general medicine services at a large academic medical center in Chicago, USA. While the concept of multidisciplinary teams focuses on the importance of the professional background of team members, SNA emphasizes the importance of the individual and collective connections of team members, both to persons outside the team and to each other. SNA also focuses on the location of individuals and groups between other actors in the flow of information and other resources within larger organizational networks. We hypothesize that external connections may be most important when the collection or dissemination of information or influence are the greatest concerns, while the relationship of team members to each other may matter most when internal coordination, knowledge sharing, and within-group communication are most important.

Picrotoxin is a plant alkaloid that is often used to block the activity of neuronal GABA and glycine receptors. However, the mechanism by which picrotoxin inhibits these receptors is still in debate. In this study, we investigated the picrotoxin inhibition on perch-subunits expressed heterologously in Xenopus laevis oocytes, and on native GABA C receptors of perch bipolar cells. Both competitive and noncompetitive mechanisms were observed for picrotoxin inhibition of the GABA C receptor. In oocytes expressing the 1A subunit, terminating simultaneously the coapplication of GABA and picrotoxin induced a large rebound of membrane current. In addition, picrotoxin significantly accelerated the kinetics of GABA responses, particularly in the relaxation (offset) phase of GABA currents. Both current rebound and the large acceleration of GABA relaxation were unique to picrotoxin inhibition and were not observed with the competitive antagonist (1,2,5,6-tetrahydropyridin-4-yl)-methylphosphinic acid or the allosteric modulator zinc. The change in kinetics induced by picrotoxin was also observed on receptors formed by other GABA subunits, as well as on the GABA C receptors of retinal bipolar cells. Based on these observations, we proposed a model in which picrotoxin binds to the GABA C receptor in both channel open and closed states. Overall, this model provides a remarkably good approximation of the experimental findings we observed for picrotoxin inhibition of GABA C receptors. These results support an allosteric mechanism of picrotoxin inhibition of ligand-gated chloride channels.

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