The role of health care organizations in patient engagement: Mechanisms to support a strong relationship between patients and clinicians.

BACKGROUND: Patient engagement (PE) is critical to improving patient experience and outcomes, as well as clinician work life and lowering health care costs, yet health care organizations (HCOs) have limited guidance about how to support PE. The engagement capacity framework considers the context of engagement and examines precursors to engagement, including patients' self-efficacy, resources, willingness, and capabilities. PURPOSE: The aim of this study was to explore clinician and patient perspectives related to mechanisms through with the HCOs can facilitate PE through the lens of the engagement capacity framework. METHODOLOGY/APPROACH: We administered an online open-ended survey to clinicians and patient advisors across the United States, including questions focused on the influences of, barriers to, and skills and tools required for PE. A common theme emerged focusing on the role of HCOs in facilitating engagement. Our analysis examined all responses tagged with the "health care system" code. RESULTS: Over 750 clinicians and patient advisors responded to our survey. Respondents identified offering advice and support for patients to manage their care (self-efficacy), providing tools to facilitate communication (resources), working to encourage connection with patients (willingness), and training for HCO employees in cultural competency and communication skills (capabilities) as important functions of HCOs related to engagement. CONCLUSION: HCOs play an important role in supporting a strong partnership between the patient and clinicians. Our study identifies important mechanisms through which HCOs can fulfill this role. PRACTICE IMPLICATIONS: HCO leadership and administration can help establish the culture of care provided. Policies and initiatives that provide appropriate communication tools and promote culturally competent care can increase engagement.

Heterogeneity at work: implications of the 2012 Clinical Translational Science Award evaluators survey.

The Clinical and Translational Science Award (CTSA) program is an ambitious multibillion dollar initiative sponsored by the National Institutes of Health (NIH) organized around the mission of facilitating the improved quality, efficiency, and effectiveness of translational health sciences research across the country. Although the NIH explicitly requires internal evaluation, funded CTSA institutions are given wide latitude to choose the structure and methods for evaluating their local CTSA program. The National Evaluators Survey was developed by a peer-led group of local CTSA evaluators as a voluntary effort to understand emerging differences and commonalities in evaluation teams and techniques across the 61 CTSA institutions funded nationwide. This article presents the results of the 2012 National Evaluators Survey, finding significant heterogeneity in evaluation staffing, organization, and methods across the 58 CTSAs institutions responding. The variety reflected in these findings represents both a liability and strength. A lack of standardization may impair the ability to make use of common metrics, but variation is also a successful evolutionary response to complexity. Additionally, the peer-led approach and simple design demonstrated by the questionnaire itself has value as an example of an evaluation technique with potential for replication in other areas across the CTSA institutions or any large-scale investment where multiple related teams across a wide geographic area are given the latitude to develop specialized approaches to fulfilling a common mission.

CCAAT enhancer binding protein-beta regulates matrix metalloproteinase-1 expression in interleukin-1beta-stimulated A549 lung carcinoma cells.

Matrix metalloproteinase-1 (MMP-1) is an inflammation-inducible neutral protease that mediates extracellular matrix remodeling and promotes tumor invasion. In this study, we examined the activation of MMP-1 gene expression in A549 lung carcinoma cells stimulated with the inflammatory cytokine interleukin-1beta (IL-1beta). We found that MMP-1 mRNA levels were maximal following 16 hours of IL-1beta stimulation and that this correlated with the expression of the transcription factor CCAAT enhancer-binding protein-beta (CEBPB). Knockdown of CEBPB expression with short hairpin RNA abrogated the expression of MMP-1, MMP-3, and MMP-10 in IL-1beta-stimulated A549 cells. An established CEBP element in the MMP-1 promoter was found to be required for basal and IL-1beta-induced transcription. Electrophoresis mobility shift assays showed that CEBPB binds to this promoter element maximally 16 hours after IL-1beta stimulation. DNA affinity chromatography studies showed that the LAP1, LAP2, and LIP isoforms of CEBPB bind to the IL-1beta-responsive CEBPB site in the MMP-1 promoter. Exogenous expression of the LAP1 and LAP2 isoforms stimulated the MMP-1 promoter, whereas LIP had no effect. Phosphorylation of CEBPB at Thr(235) peaked at 16 hours in IL-1beta-stimulated cells. The MEK inhibitor U0126 inhibited this phosphorylation and reduced MMP-1 gene induction. These studies establish CEBPB as an important mediator of metalloproteinase gene activation during inflammatory responses in lung cancer cells and highlight the different regulatory roles of CEBPB isoforms.