Outcomes Standardisation Project (OSP) for Continuing Medical Education (CE/CME) Professionals: Background, Methods, and Initial Terms and Definitions.

Despite an increased focus and urgency for CE/CME professionals to effectively and systematically assess the impact of their educational interventions, the community has struggled to do so. This struggle is in large part due to the lack of a standardised outcomes language and a set of unified approaches to measure and communicate impact. In the spring of 2018, a group of volunteer educational research scientists and CE/CME professionals established a rigorous consensus-building process in an effort to address this need. This report describes the background, methods and first-year output (Glossary V1) of the Outcomes Standardisation Project (OSP); begins to introduce examples of how the OSP Glossary V1 may support the CE/CME professional community and concludes with plans for the future of establishing a common framework for the profession.

The Rise and Stall of eLearning: Best Practices for Technology-Supported Education.

eLearning is a commonly used term in education today, but what does it mean? This article explores issues that nurse planners and administrators need to be aware of in planning how technology-based education is most effectively delivered.

Flipping the classroom: a data-driven model for nursing education.

Structured, blended learning models have been developed to help participants more actively engage in learning experiences, as opposed to traditional didactic sessions. A flipped classroom model allows learners to build on self-directed online prework in an interactive and collaborative learning laboratory.

Understanding the factors that influence the adoption and meaningful use of social media by physicians to share medical information.

BACKGROUND: Within the medical community there is persistent debate as to whether the information available through social media is trustworthy and valid, and whether physicians are ready to adopt these technologies and ultimately embrace them as a format for professional development and lifelong learning. OBJECTIVE: To identify how physicians are using social media to share and exchange medical information with other physicians, and to identify the factors that influence physicians' use of social media as a component of their lifelong learning and continuing professional development. METHODS: We developed a survey instrument based on the Technology Acceptance Model, hypothesizing that technology usage is best predicted by a physician's attitudes toward the technology, perceptions about the technology's usefulness and ease of use, and individual factors such as personal innovativeness. The survey was distributed via email to a random sample of 1695 practicing oncologists and primary care physicians in the United States in March 2011. Responses from 485 physicians were analyzed (response rate 28.61%). RESULTS: Overall, 117 of 485 (24.1%) of respondents used social media daily or many times daily to scan or explore medical information, whereas 69 of 485 (14.2%) contributed new information via social media on a daily basis. On a weekly basis or more, 296 of 485 (61.0%) scanned and 223 of 485 (46.0%) contributed. In terms of attitudes toward the use of social media, 279 of 485 respondents (57.5%) perceived social media to be beneficial, engaging, and a good way to get current, high-quality information. In terms of usefulness, 281 of 485 (57.9%) of respondents stated that social media enabled them to care for patients more effectively, and 291 of 485 (60.0%) stated it improved the quality of patient care they delivered. The main factors influencing a physician's usage of social media to share medical knowledge with other physicians were perceived ease of use and usefulness. Respondents who had positive attitudes toward the use of social media were more likely to use social media and to share medical information with other physicians through social media. Neither age nor gender had a significant impact on adoption or usage of social media. CONCLUSIONS: Based on the results of this study, the use of social media applications may be seen as an efficient and effective method for physicians to keep up-to-date and to share newly acquired medical knowledge with other physicians within the medical community and to improve the quality of patient care. Future studies are needed to examine the impact of the meaningful use of social media on physicians' knowledge, attitudes, skills, and behaviors in practice.

The Na+/Ca2+ exchanger/SR Ca2+ ATPase transport capacity regulates the contractility of normal and hypertrophied feline ventricular myocytes.

BACKGROUND: Pressure overload leads to cardiac hypertrophy, which is often followed by heart failure. We tested the hypothesis that depressed contractility in this process results from an imbalance in Ca 2+ transport by the sarcoplasmic reticulum (SR) Ca2+ ATPase (SERCA) and the sarcolemmal Na+/Ca2+ exchanger (NCX). METHODS AND RESULTS: Left ventricular (LV) myocytes (n = 79) from 12 normal (N) and 5 hypertrophied (LVH, by aortic banding) feline hearts were studied. Adenoviral gene transfer was used to introduce green fluorescent protein (GFP), SERCA2, and NCX into N and LVH myocytes. Contraction (videomicroscopy) and Ca2+ transients (Fluo-3) were measured in steady state and after rest periods of 2 to 120 seconds (rest decay and potentiation). LVH hearts were significantly larger than N (7.1 +/- 1.4 versus 4.2 +/- 0.2 g/kg). SERCA protein was significantly less abundant in LVH versus N. Steady state contractions and Ca2+ transients of LVH-GFP myocytes decayed more slowly and rest decay of contractility was more pronounced compared with N-GFP. Infection of LVH (and N) myocytes with SERCA increased basal contractility and reduced rest decay. Infection of LVH myocytes with NCX almost abolished contraction and in N myocytes reduced contractility and increased rest decay. CONCLUSION: These findings suggest that an imbalance of Ca2+ transport by SERCA and the NCX produces the characteristic contractile abnormalities of hypertrophied cardiac myocytes.

Gene expression profiling during the transition to failure in TNF-alpha over-expressing mice demonstrates the development of autoimmune myocarditis.

Transgenic mice with cardiac-specific over-expression of tumor necrosis factor-alpha (TNF1.6) progress to dilated heart failure. A significant inflammatory response precedes functional deterioration, and may contribute to cardiac damage in this model. To evaluate the underlying molecular mechanisms, we assessed the gene expression in six groups of mouse hearts defined by age, gender, and phenotype (n = 3/group) using Affymetrix microarray analysis. Phenotype was defined as compensated (in young TNF1.6) or decompensated (in older TNF1.6) via echocardiogram. Of the >1000 transcripts altered in the compensated hearts (fold change > 2, P < 0.05 vs. wild-type (WT)), 102 were identified as immune response genes, 20 of which function in antigen presentation and processing. When comparing the compensated and decompensated hearts, >50 genes were differentially regulated, including seven immunoglobulin genes. Real-time reverse transcriptase-polymerase chain reaction and cDNA microarray confirmed the Affymetrix data. Mac3+ macrophages, CD4+ T and CD45/B220+ B-cells were identified in both compensated and decompensated hearts. However, a large amount of IgG was found deposited in areas devoid of B-lymphocytes in the myocardium of decompensated TNF1.6 mice; no such accumulation was seen in the compensated or age-matched controls. Furthermore, nuclei density analyses showed a two-fold increase in the myocardium of both compensated and decompensated TNF1.6 mice (vs. WT). This study suggests that TNF-alpha over-expression activates not only the inflammatory response, but also humoral immune responses within the transgenic hearts. The autoimmune response occurs concomitantly with cardiac decompensation and may participate in triggering the transition to failure in TNF1.6 mice.

Tumor necrosis factor receptors 1 and 2 differentially regulate survival, cardiac dysfunction, and remodeling in transgenic mice with tumor necrosis factor-alpha-induced cardiomyopathy.

BACKGROUND: Tumor necrosis factor (TNF)-alpha plays a pathophysiological role in heart failure. Although both TNF receptor 1 (TNFR1) and 2 (TNFR2) are present in the heart, comparatively little is known about the role of TNFR2. METHODS AND RESULTS: We bred TNFR1-knockout (KO) or TNFR2KO mice to transgenic (TG) mice with cardiac-specific overexpression of TNF-alpha and analyzed resultant progeny. Six groups of male and female mice were studied: wild type (WT) with wild receptors (WT/W), TG with wild receptors (TG/W), TG with heterozygous receptor KO (TG/R1+/- or TG/R2+/-), and TG with homozygous receptor KO (TG/R1-/- or TG/R2-/-). Both male and female TG mice displayed cardiac hypertrophy, dilation, and reduced cardiac function. Male TG mice were more severely affected than genotypically matched females and died of heart failure at a younger age. Survival, cardiac function, and remodeling of TG/R1+/- and TG/R1-/- mice were improved relative to TG/W mice in both males and females. However, the survival of female TG/R2+/- and TG/R2-/- mice was worse than that of TG/W mice, with increased left ventricular dimension and left ventricular weight/body weight ratios. The cardiac TNF-alpha protein level was upregulated in TG/R1-/- and TG/R2-/- compared with TG/W mice, whereas the level of TNF receptors was not downregulated in TG/W relative to WT/W mice. CONCLUSIONS: Ablation of the TNFR2 gene exacerbates heart failure and reduces survival, whereas ablation of TNFR1 blunts heart failure and improves survival. Signaling via TNFR2 may play a cardioprotective role in the pathogenesis of cytokine-mediated heart failure.

The balance between pro-apoptotic and anti-apoptotic pathways in the failing myocardium.

The purpose of this review is to highlight those circulating molecules, membrane receptors, and signaling pathways that initiate, potentiate, or conversely, inhibit apoptosis within cardiomyocytes. This review focuses on pathways directly related to the failing heart and discusses the limitations of current methodologies for assessing cardiomyocellular apoptosis. It is important to note that the adrenergic, reactive oxygen species, and proinflammatory cytokine signaling pathways are not the only pro-apoptotic pathways active in the myocardium, nor are IL-6-related cytokine, calcineurin, and IGF-1/PI3K/Akt signaling pathways the only anti-apoptotic pathways active in the myocardium. However, they are among the best-characterized apoptosis-mediating pathways and therefore they may serve as foundation for future studies aimed at identifying novel apoptotic regulating pathways active in cardiomyocytes. Considering the short history of studying cardiomyocellular apoptosis, a tremendous body of knowledge has been collected. Understandably, much more work remains. Tomorrow's studies must (1) continue to examine the signaling pathways mediating cardiomyocellular apoptosis by focusing on the links to the ubiquitous apoptosis effectors, (2) use the expanding body of knowledge to develop more specific inhibitors of apoptosis, and then (3) confirm the causal relationship of cardiomyocellular apoptosis and cardiac dysfunction in physiologic models of cardiac challenge.

Unloading-induced remodeling in the normal and hypertrophic left ventricle.

To date, no study has assessed the degree of similarity between left ventricular (LV) reverse remodeling and atrophic remodeling. Stable LV hypertrophy was induced by creation of an arteriovenous fistula (AVF) in Lewis rats (32 days). LV unloading was induced by heterotopic transplantation of normal (NL-HT) and/or hypertrophic (AVF-HT) hearts (7 days). We compared indexes of remodeling in AVF, NL-HT, and AVF-HT groups with those of normal controls. LV unloading induced decreases in cardiomyocyte size in NL-HT and AVF-HT hearts. NL-HT and AVF-HT LV were both characterized by relative increases in collagen concentration that were largely a reflection of decreases in myocyte volume. NL-HT and AVF-HT LV were associated with similar increases in matrix metalloproteinase (MMP-2 and -9) zymographic activity, without change in the abundance of the tissue inhibitors of the MMPs. In contrast, AVF-HT, but not NL-HT, was associated with a dramatic increase in collagen cross-linking. Our findings suggest an overall similarity in the response of the normal and hypertrophic LV to surgical unloading. However, the dramatic increase in collagen cross-linking after just 1 wk of unloading suggests a potential difference in the dynamics of collagen metabolism between the two models. Further studies will be required to determine the precise molecular mechanisms responsible for these differences in extracellular matrix regulation. However, with respect to these and related issues, heterotopic transplantation of hypertrophied hearts will be a useful small animal model for defining mechanisms of myocyte-matrix interactions during decreased loading conditions.