Educator Toolkits on Second Victim Syndrome, Mindfulness and Meditation, and Positive Psychology: The 2017 Resident Wellness Consensus Summit.

INTRODUCTION: Burnout, depression, and suicidality among residents of all specialties have become a critical focus of attention for the medical education community. METHODS: As part of the 2017 Resident Wellness Consensus Summit in Las Vegas, Nevada, resident participants from 31 programs collaborated in the Educator Toolkit workgroup. Over a seven-month period leading up to the summit, this workgroup convened virtually in the Wellness Think Tank, an online resident community, to perform a literature review and draft curricular plans on three core wellness topics. These topics were second victim syndrome, mindfulness and meditation, and positive psychology. At the live summit event, the workgroup expanded to include residents outside the Wellness Think Tank to obtain a broader consensus of the evidence-based toolkits for these three topics. RESULTS: Three educator toolkits were developed. The second victim syndrome toolkit has four modules, each with a pre-reading material and a leader (educator) guide. In the mindfulness and meditation toolkit, there are three modules with a leader guide in addition to a longitudinal, guided meditation plan. The positive psychology toolkit has two modules, each with a leader guide and a PowerPoint slide set. These toolkits provide educators the necessary resources, reading materials, and lesson plans to implement didactic sessions in their residency curriculum. CONCLUSION: Residents from across the world collaborated and convened to reach a consensus on high-yield-and potentially high-impact-lesson plans that programs can use to promote and improve resident wellness. These lesson plans may stand alone or be incorporated into a larger wellness curriculum.

αv integrins: key regulators of tissue fibrosis.

Chronic tissue injury with fibrosis results in the disruption of tissue architecture, organ dysfunction and eventual organ failure. Therefore, the development of effective anti-fibrotic therapies is urgently required. During fibrogenesis, complex interplay occurs between cellular and extracellular matrix components of the wound healing response. Integrins, a family of transmembrane cell adhesion molecules, play a key role in mediating intercellular and cell-matrix interactions. Thus, integrins provide a major node of communication between the extracellular matrix, inflammatory cells, fibroblasts and parenchymal cells and, as such, are intimately involved in the initiation, maintenance and resolution of tissue fibrosis. Modulation of members of the αv integrin family has exhibited profound effects on fibrosis in multiple organs and disease states. In this review, we discuss the current knowledge of the mechanisms of αv-integrin-mediated regulation of fibrogenesis and show that the therapeutic targeting of specific αv integrins represents a promising avenue to treat patients with a broad range of fibrotic diseases.

Hepatic stellate cells: central modulators of hepatic carcinogenesis.

Hepatocellular carcinoma (HCC) represents the second most common cause of cancer-related death worldwide, and is increasing in incidence. Currently, our therapeutic repertoire for the treatment of HCC is severely limited, and therefore effective new therapies are urgently required. Recently, there has been increasing interest focusing on the cellular and molecular interactions between cancer cells and their microenvironment. HCC represents a unique opportunity to study the relationship between a diseased stroma and promotion of carcinogenesis, as 90% of HCCs arise in a cirrhotic liver. Hepatic stellate cells (HSC) are the major source of extracellular proteins during fibrogenesis, and may directly, or via secreted products, contribute to tumour initiation and progression. In this review we explore the complex cellular and molecular interplay between HSC biology and hepatocarcinogenesis. We focus on the molecular mechanisms by which HSC modulate HCC growth, immune cell evasion and angiogenesis. This is followed by a discussion of recent progress in the field in understanding the mechanistic crosstalk between HSC and HCC, and the pathways that are potentially amenable to therapeutic intervention. Furthermore, we summarise the exciting recent developments in strategies to target HSC specifically, and novel techniques to deliver pharmaceutical agents directly to HSC, potentially allowing tailored, cell-specific therapy for HCC.

Cre-ativity in the liver: transgenic approaches to targeting hepatic nonparenchymal cells.

Rapid evolution in transgenic (Tg) mouse technology now permits cell-specific and temporal control of fluorescent cell-labeling and gene inactivation. Here, we discuss the principal strategies that have been utilized to target, label, and manipulate hepatic nonparenchymal cells, with emphasis on the utility of constitutive and inducible Cre-lox systems. We summarize key findings of studies employing Tg technology to target hepatic stellate cells, myofibroblasts, liver sinusoidal endothelial cells, and macrophages to illustrate the power of these approaches in identifying cell-specific molecular mechanisms critical to the pathophysiology of liver disease. Increasing adoption of Tg techniques will help to answer fundamental questions regarding the pathogenesis of hepatic diseases and provide the mechanistic rationale to allow identification of novel drug targets, ultimately translating into effective therapies for patients with liver disease.