Building cohesion in distributed telemedicine teams: findings from the Department of Veterans Affairs National Telestroke Program.

BACKGROUND: As telemedicine adoption increases, so does the importance of building cohesion among physicians in telemedicine teams. For example, in acute telestroke services, stroke specialists provide rapid remote stroke assessment and treatment to patients at hospitals without stroke specialty care. In the National Telestroke Program (NTSP) of the U.S. Department of Veterans Affairs, a virtual (distributed) hub of stroke specialists throughout the country provides 24/7 consultations nationwide. We examined how these specialists adapted to distributed teamwork, and we identified cohesion-related factors in program development and support. METHODS: We studied the virtual hub of stroke specialists employed by the NTSP. Semi-structured, confidential interviews with stroke specialists in the virtual hub were recorded and transcribed. We explored the extent to which these specialists had developed a sense of shared identity and team cohesion, and we identified factors in this development. Using a qualitative approach with constant comparison methods, two researchers coded each interview transcript independently using a shared codebook. We used matrix displays to identify themes, with special attention to team cohesion, communication, trust, and satisfaction. RESULTS: Of 13 specialists with at least 8 months of NTSP practice, 12 completed interviews; 7 had previously practiced in telestroke programs in other healthcare systems. Interviewees reported high levels of trust and team cohesion, sometimes even more with their virtual colleagues than with co-located colleagues. Factors facilitating perceived team cohesion included a weekly case conference call, a sense of transparency in discussing challenges, engagement in NTSP development tasks, and support from the NTSP leadership. Although lack of in-person contact was associated with lower cohesion, annual in-person NTSP meetings helped mitigate this issue. Despite technical challenges in establishing a new telehealth system within existing national infrastructure, providers reported high levels of satisfaction with the NTSP. CONCLUSION: A virtual telestroke hub can provide a sense of team cohesion among stroke specialists at a level comparable with a standard co-located practice. Engaging in transparent discussion of challenging cases, reviewing new clinical evidence, and contributing to program improvements may promote cohesion in distributed telemedicine teams.

The Bacillus Subtilis K-State Promotes Stationary-Phase Mutagenesis via Oxidative Damage.

Bacterial cells develop mutations in the absence of cellular division through a process known as stationary-phase or stress-induced mutagenesis. This phenomenon has been studied in a few bacterial models, including Escherichia coli and Bacillus subtilis; however, the underlying mechanisms between these systems differ. For instance, RecA is not required for stationary-phase mutagenesis in B. subtilis like it is in E. coli. In B. subtilis, RecA is essential to the process of genetic transformation in the subpopulation of cells that become naturally competent in conditions of stress. Interestingly, the transcriptional regulator ComK, which controls the development of competence, does influence the accumulation of mutations in stationary phase in B. subtilis. Since recombination is not involved in this process even though ComK is, we investigated if the development of a subpopulation (K-cells) could be involved in stationary-phase mutagenesis. Using genetic knockout strains and a point-mutation reversion system, we investigated the effects of ComK, ComEA (a protein involved in DNA transport during transformation), and oxidative damage on stationary-phase mutagenesis. We found that stationary-phase revertants were more likely to have undergone the development of competence than the background of non-revertant cells, mutations accumulated independently of DNA uptake, and the presence of exogenous oxidants potentiated mutagenesis in K-cells. Therefore, the development of the K-state creates conditions favorable to an increase in the genetic diversity of the population not only through exogenous DNA uptake but also through stationary-phase mutagenesis.

Stationary-Phase Mutagenesis in Stressed Bacillus subtilis Cells Operates by Mfd-Dependent Mutagenic Pathways.

In replication-limited cells of Bacillus subtilis, Mfd is mutagenic at highly transcribed regions, even in the absence of bulky DNA lesions. However, the mechanism leading to increased mutagenesis through Mfd remains currently unknown. Here, we report that Mfd may promote mutagenesis in nutritionally stressed B. subtilis cells by coordinating error-prone repair events mediated by UvrA, MutY and PolI. Using a point-mutated gene conferring leucine auxotrophy as a genetic marker, it was found that the absence of UvrA reduced the Leu⁺ revertants and that a second mutation in mfd reduced mutagenesis further. Moreover, the mfd and polA mutants presented low but similar reversion frequencies compared to the parental strain. These results suggest that Mfd promotes mutagenic events that required the participation of NER pathway and PolI. Remarkably, this Mfd-dependent mutagenic pathway was found to be epistatic onto MutY; however, whereas the MutY-dependent Leu⁺ reversions required Mfd, a direct interaction between these proteins was not apparent. In summary, our results support the concept that Mfd promotes mutagenesis in starved B. subtilis cells by coordinating both known and previously unknown Mfd-associated repair pathways. These mutagenic processes bias the production of genetic diversity towards highly transcribed regions in the genome.

Mfd and transcriptional derepression cause genetic diversity in Bacillus subtilis.

Scientists have been aware for many years of genetic programs that get activated under stress and produce genetic variants in cells that escape non-proliferating conditions. These programs are well conserved in all organisms and expand our view of evolution. They mediate genome instability, create diversity in antibody formation, expand metabolism and increase fitness of pathogens within host environments. Error-prone DNA replication and repair are genetic variability-causing agents that get stimulated by the onset of cellular stresses. Embedded in these programs is the ability to limit mutagenesis to defined genomic regions and times, ensuring integrity of most of the genome. Recent evidence suggests that factors involved in RNA polymerase (RNAP) processivity or transcriptional derepression contribute to the generation of stress-induced mutations. In Bacillus subtilis, transcription-associated mutagenesis has been shown to be independent of recombination-dependent repair and, in some cases, of the Y DNA polymerases. Central to stationary-phase mutagenesis in B. subtilis is the requirement for Mfd, transcription coupling repair factor, which suggests a novel mechanism from those described in other model systems.