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Our modern-day frenetic healthcare culture has progressed to a state where healthcare professionals tend to detach themselves from the emotions of their patients/clients, rather than embed compassion into their daily practice. The AMS Phoenix Project: A Call to Caring was implemented with the goal to instil and sustain empathy and compassion in environments where clinicians learn and work. The purpose of this study is to report on how an interprofessional community of practice (CoP) of healthcare educators can contribute to a cultural shift in promoting and delivering compassion in healthcare through health professionals education. Using an imaginative creative autoethnography that adopts a narrative design through graphic illustrations, data were collected from 25 members of the Phoenix@Queen’s CoP during a 1-day retreat. Data collection included a graphic recorder who visually depicted all retreat dialogue, field notes that highlighted emergent themes and artefacts produced during the day. Audio recordings of the discussions were used as secondary sources of data. Using thematic analysis, three themes emerged: the call to caring is a long and winding road with many barriers and rewards; CoP members experienced personal growth in and through the community; and the Phoenix@Queen’s CoP matters in terms of professional relationships, leadership and moving forward a shared agenda about practising compassionate healthcare. This study describes the development of a CoP that moves away from traditional committees and discussions to an experiential creation of connections and shared meaning by its members. By using autoethnography, and by demonstrating how graphic illustration can be an innovative and creative method for recording and interpreting group discussions, we have demonstrated the accelerated development of an authentic CoP. With a richer and more authentic community, the shared goals of healthcare professional educators are more likely to be achieved.

AIMS: The human ether-a-go-go-related gene (hERG) encodes the rapidly activating delayed rectifier potassium channel (I(Kr)). Malfunction of hERG/I(Kr) is the primary cause of acquired long QT syndrome (LQTS), an electrical disorder of the heart that can cause arrhythmias and sudden death. Patients with autoimmune diseases display a high incidence of LQTS. While dysfunction of hERG channels induced by autoantibodies such as anti-Ro52 may play a role in this pathology, the underlying mechanisms are not well understood. Here, we investigated the acute and chronic effects of anti-Ro52 antibody on hERG channels stably expressed in human embryonic kidney (hERG-HEK) 293 cells as well as I(Kr) in neonatal rat ventricular myocytes. METHODS AND RESULTS: Using whole-cell patch clamp, western blot analyses, and immunocytochemistry, we found that a 12-h treatment of hERG-HEK cells with patients’ sera containing anti-Ro52 autoantibody decreased the hERG current (I(hERG)) by 32% compared to cells treated with autoantibody-negative patients’ sera. Commercial anti-Ro52 antibody at 100 µg/mL did not acutely block I(hERG). Instead, a 12-h treatment with anti-Ro52 antibody at a concentration of 4 µg/mL significantly reduced mature hERG protein expression and I(hERG). Specifically, anti-Ro52 antibody did not acutely block hERG current but chronically facilitated hERG endocytic degradation. The extracellular S5-pore linker of hERG, which forms the turret of the channel on the outside of the cell, is the target region for anti-Ro52-mediated hERG reduction since its replacement with the analogous region of EAG abolished the anti-Ro52 effect. In neonatal rat ventricular myocytes, 100 µg/mL anti-Ro52 antibody did not acutely block I(Kr), but a 12-h treatment of cells with 4 µg/mL anti-Ro52 antibody selectively reduced I(Kr) and prolonged the action potential duration. CONCLUSIONS: Our results indicate that anti-Ro52 antibody acts on the hERG S5-pore linker to chronically decrease hERG expression and current. These findings provide novel insights into hERG regulation and anti-Ro52 antibody-associated LQTS.