Publications

PURPOSE

Health care systems increasingly demand health professionals who can lead interdisciplinary teams. While physicians recognize the importance of leadership skills, few receive formal instruction in this area. This paper aims to describe how the Student Leadership Committee (SLC) at the Harvard Medical School Center for Primary Care responded to this need by creating a leadership curriculum for health professions students.

DESIGN/METHODOLOGY/APPROACH

The SLC designed an applied longitudinal leadership curriculum and taught it to medical, dentistry, nursing, public health and business students during monthly meetings over two academic years. The perceptions of the curriculum were assessed via a retrospective survey and an assessment of team functioning.

FINDINGS

Most teams met their project goals and students felt that their teams were effective. The participants reported increased confidence that they could create change in healthcare and an enhanced desire to hold leadership positions. The sessions that focused on operational skills were especially valued by the students.

PRACTICAL IMPLICATIONS

This case study presents an effective approach to delivering leadership training to health professions students, which can be replicated by other institutions.

SOCIAL IMPLICATIONS

Applied leadership training empowers health professions students to improve the health-care system and prepares them to be more effective leaders of the future health-care teams. The potential benefits of improved health-care leadership are numerous, including better patient care and improved job satisfaction among health-care workers.

ORIGINALITY/VALUE

Leadership skills are often taught as abstract didactics. In contrast, the approach described here is applied to ongoing projects in an interdisciplinary setting, thereby preparing students for real-world leadership positions.

Natural killer (NK) cells are innate lymphoid cells that have been increasingly recognised as important in lung allograft tolerance and immune defence. These cells evolved to recognise alterations in self through a diverse set of germline-encoded activating and inhibitory receptors and display a broad range of effector functions that play important roles in responding to infections, malignancies and allogeneic tissue. Here, we review NK cells, their diverse receptors and the mechanisms through which NK cells are postulated to mediate important lung transplant clinical outcomes. NK cells can promote tolerance, such as through the depletion of donor antigen-presenting cells. Alternatively, these cells can drive rejection through cytotoxic effects on allograft tissue recognised as 'non-self' or 'stressed', via killer cell immunoglobulin-like receptor (KIR) or NKG2D receptor ligation, respectively. NK cells likely mediate complement-independent antibody-mediated rejection of allografts though CD16A Fc receptor-dependent activation induced by graft-specific antibodies. Finally, NK cells play an important role in response to infections, particularly by mediating cytomegalovirus infection through the CD94/NKG2C receptor. Despite these sometimes-conflicting effects on allograft function, enumeration of NK cells may have an important role in diagnosing allograft dysfunction. While the effects of immunosuppression agents on NK cells may currently be largely unintentional, further understanding of NK cell biology in lung allograft recipients may allow these cells to serve as biomarkers of graft injury and as therapeutic targets.

MESP1 is a key transcription factor in development of early cardiovascular tissue and it is required for induction of the cardiomyocyte (CM) gene expression program, but its role in vascular development is unclear. Here, we used inducible CRISPRi knock-down of MESP1 to analyze the molecular processes of the early differentiation stages of human induced pluripotent stem cells into mesoderm and subsequently vascular progenitor cells. We found that expression of the mesodermal marker, BRACHYURY (encoded by T) was unaffected in MESP1 knock-down cells as compared to wild type cells suggesting timely movement through the primitive streak whereas another mesodermal marker MIXL1 was slightly, but significantly decreased. In contrast, the expression of the vascular cell surface marker KDR was decreased and CD31 and CD34 expression were substantially reduced in MESP1 knock-down cells supporting inhibition or delay of vascular specification. In addition, mRNA microarray data revealed several other altered gene expressions including the EMT regulating transcription factors SNAI1 and TWIST1, which were both significantly decreased indicating that MESP1 knock-down cells are less likely to undergo EMT during vascular progenitor differentiation. Our study demonstrates that while leaving primitive streak markers unaffected, MESP1 expression is required for timely vascular progenitor specification. Thus, MESP1 expression is essential for the molecular features of early CM, EC and VSMC lineage specification.