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Background Accreditation is considered an essential ingredient for an effective system of health professions education (HPE) globally. While accreditation systems exist in various forms worldwide, there has been little written about the contemporary enterprise of accreditation and even less about its role in improving health care outcomes. We set out to 1) identify a global, contemporary definition of accreditation in the health professions, 2) describe the relationship of educational accreditation to health care outcomes, 3) identify important questions and recurring issues in twenty-first century HPE accreditation, and 4) propose a framework of essential ingredients in present-day HPE accreditation. Methods We identified health professions accreditation leaders via a literature search and a Google search of HPE institutions, as well as by accessing the networks of other leaders. These leaders were invited to join an international consensus consortium to advance the scholarship and thinking about HPE accreditation. We describe the consensus findings from the International Health Professions Accreditation Outcomes Consortium (IHPAOC). Results We define accreditation as the process of formal evaluation of an educational program, institution, or system against defined standards by an external body for the purposes of quality assurance and enhancement. In the context of HPE, accreditation is distinct from other forms of program evaluation or research. Accreditation can enhance health care outcomes because of its ability to influence and standardize the quality of training programs, continuously enhance curriculum to align with population needs, and improve learning environments. We describe ten fundamental and recurring elements of accreditation systems commonly found in HPE and provide an overview of five emerging developments in accreditation in the health professions based on the consensus findings. Conclusions Accreditation has taken on greater importance in contemporary HPE. These consensus findings provide frameworks of core elements of accreditation systems and both recurring and emerging design issues. HPE scholars, educators, and leaders can build on these frameworks to advance research, development, and operation of high-quality accreditation systems worldwide.

Localized scleroderma (LS) is a complex disease characterized by a mixture of inflammation and fibrosis of the skin that, especially in the pediatric population, also affects extracutaneous tissues ranging from muscle to the central nervous system. Although developmental origins have been hypothesized, evidence points to LS as a systemic autoimmune disorder, as there is a strong correlation to family history of autoimmune disease, the presence of shared HLA types with rheumatoid arthritis, high frequency of auto-antibodies, and elevated circulating chemokines and cytokines associated with T-helper cell, IFNγ, and other inflammatory pathways. This inflammatory phenotype of the peripheral blood is reflected in the skin via microarray, RNA Sequencing and tissue staining. Research is underway to identify the key players in the pathogenesis of LS, but close approximation of inflammatory lymphocytic and macrophage infiltrate with collagen and fibroblasts deposition supports the notion that LS is a disease of inflammatory driven fibrosis. The immune system is dynamic and undergoes changes during childhood, and we speculate on how the unique features of the immune system in childhood could potentially contribute to some of the differences in LS between children and adults. Interestingly, the immune phenotype in pediatric LS resembles to some extent the healthy adult cellular phenotype, possibly supporting accelerated maturation of the immune system in LS. We discuss future directions in better understanding the pathophysiology of and how to better treat pediatric LS.

Background Accreditation is a key feature of many medical education systems, helping to ensure that programs teach and assess learners according to applicable standards, provide optimal learning environments, and produce professionals who are competent to practise in challenging and evolving health care systems. Although most medical education accreditation systems apply similar standards domains and process elements, there can be substantial variation among accreditation systems at the level of design and implementation. A discussion group at the 2013 World Summit on Outcomes-Based Accreditation examined best practices in health professional education accreditation systems and identified that the literature examining the effectiveness of different approaches to accreditation is scant. Although some frameworks for accreditation design do exist, they are often specific to one phase of the medical education continuum. Main text This paper attempts to define a framework for the operational design of medical education accreditation that articulates design options as well as their contextual and practical implications. It assumes there is no single set of best practices in accreditation system development but, rather, an underlying set of design decisions. A “fit for purpose” approach aims to ensure that a system, policy, or program is designed and operationalized in a manner best suited to local needs and contexts. This approach is aligned with emerging models for education and international development that espouse decentralization. Conclusion The framework highlights that, rather than a single best practice, variation among accreditation systems is appropriate provided that is it tailored to the needs of local contexts. Our framework is intended to provide guidance to administrators, policy-makers, and educators regarding different approaches to medical education accreditation and their applicability and appropriateness in local contexts.

Juvenile-onset systemic sclerosis (jSSc) is a rare and severe autoimmune disease with associated life-threatening organ inflammation and evidence of fibrosis. The organ manifestations of jSSc resemble adult SSc, but with better outcomes and survival. The etiology of jSSc appears to reflect adult-onset SSc, with similar inflammatory mediators and autoantibodies, but with a significant population of children with uncharacterized anti-nuclear antibodies. The genetics of patients with jSSc differ from women with SSc, resembling instead the genes of adult males with SSc, with additional HLA genes uniquely associated with childhood-onset disease. Current treatments are aimed at inhibiting the inflammatory aspect of disease, but important mechanisms of fibrosis regulated by dermal white adipose tissue dendritic cells may provide an avenue for targeting and potentially reversing the fibrotic stage.

Cross-pollination has been associated with improved fruit set, weight, and shortened time to ripening in southern highbush blueberry [SHB ( Vaccinium corymbosum interspecific hybrids)]. Because of this, growers commonly plant two or more cultivars in small blocks to facilitate cross-pollination. However, many SHB cultivars may vary in the degree of improvement in each parameter after cross-pollination. Understanding the impacts of cross-pollination on a particular cultivar is crucial to forming planting recommendations, particularly as growers begin to transition to fields designed for machine harvest where large solid blocks would increase the harvest efficiency. The objective of this study was to examine the effects of cross- and self-pollination among 13 commonly planted or newly released SHB cultivars. Cross-pollination typically improved fruit set, fruit weight, and seed number while decreasing the average days to harvest. Cross-pollinated fruit always weighed more than self-pollinated fruit from the same cultivar, which was highly correlated to seed number per fruit. Although there was variation for each trait, interplanting with another unrelated cultivar sharing a similar bloom time remains the best recommendation to ensure early, high yield among these SHB cultivars.

The autoimmune disease lupus erythematosus (lupus) is characterized by photosensitivity, where even ambient ultraviolet radiation (UVR) exposure can lead to development of inflammatory skin lesions. We have previously shown that Langerhans cells (LCs) limit keratinocyte apoptosis and photosensitivity via a disintegrin and metalloprotease 17 (ADAM17)-mediated release of epidermal growth factor receptor (EGFR) ligands and that LC ADAM17 sheddase activity is reduced in lupus. Here, we sought to understand how the lupus skin environment contributes to LC ADAM17 dysfunction and, in the process, differentiate between effects on LC ADAM17 sheddase function, LC ADAM17 expression, and LC numbers. We show through transcriptomic analysis a shared IFN-rich environment in non-lesional skin across human lupus and three murine models: MRL/lpr, B6.Sle1yaa, and imiquimod (IMQ) mice. IFN-I inhibits LC ADAM17 sheddase activity in murine and human LCs, and IFNAR blockade in lupus model mice restores LC ADAM17 sheddase activity, all without consistent effects on LC ADAM17 protein expression or LC numbers. Anti-IFNAR-mediated LC ADAM17 sheddase function restoration is associated with reduced photosensitive responses that are dependent on EGFR signaling and LC ADAM17. Reactive oxygen species (ROS) is a known mediator of ADAM17 activity; we show that UVR-induced LC ROS production is reduced in lupus model mice, restored by anti-IFNAR, and is cytoplasmic in origin. Our findings suggest that IFN-I promotes photosensitivity at least in part by inhibiting UVR-induced LC ADAM17 sheddase function and raise the possibility that anifrolumab ameliorates lupus skin disease in part by restoring this function. This work provides insight into IFN-I-mediated disease mechanisms, LC regulation, and a potential mechanism of action for anifrolumab in lupus.

Background In recent decades, evidence-based practices (EBPs) have been broadly promoted in community behavioural health systems in the United States of America, yet reported EBP penetration rates remain low. Determining how to systematically sustain EBPs in complex, multi-level service systems has important implications for public health. This study examined factors impacting the sustainability of parent-child interaction therapy (PCIT) in large-scale initiatives in order to identify potential predictors of sustainment. Methods A mixed-methods approach to data collection was used. Qualitative interviews and quantitative surveys examining sustainability processes and outcomes were completed by participants from 12 large-scale initiatives. Results Sustainment strategies fell into nine categories, including infrastructure, training, marketing, integration and building partnerships. Strategies involving integration of PCIT into existing practices and quality monitoring predicted sustainment, while financing also emerged as a key factor. Conclusions The reported factors and strategies impacting sustainability varied across initiatives; however, integration into existing practices, monitoring quality and financing appear central to high levels of sustainability of PCIT in community-based systems. More detailed examination of the progression of specific activities related to these strategies may aide in identifying priorities to include in strategic planning of future large-scale initiatives. Trial registration ClinicalTrials.gov ID NCT02543359 ; Protocol number PRO12060529.

Child exposure to intimate partner violence (IPV) is widely acknowledged as a threat to the psycho-social and academic well-being of children. Unfortunately, as reflected in the literature, the specific link between such exposure and childhood outcomes is ambiguous. Based on a review of the literature, this article suggests that this state of affairs is due, in part, to the manner with which exposure to IPV is operationally defined. After reviewing the dominant strategies for operationally defining exposure to IPV and the problems associated with those strategies, this article reports original data contrasting three measures derived from maternal reports, three measures derived from child reports, and the limited concordance among those different indices of exposure to IPV. The implications of these findings for research on child outcomes and the clinical assessment of children who might have been exposed to IPV are discussed.

BackgroundThe autoimmune disease lupus erythematosus (lupus) is characterized by photosensitivity, where even ambient ultraviolet radiation (UVR) exposure inflames skin. Beneficial effects of anifrolumab (anti-interferon α/βreceptor (anti-IFNAR)) on lupus skin disease support a pathogenic role for IFN-I , but mechanistic understanding is limited. We have shown that Langerhans cell (LC) dysfunction contributes to photosensitivity. Healthy LCs act via a disintegrin and metalloprotease 17 (ADAM17) to release epidermal growth factor receptor (EGFR) ligands that limit UVR-induced keratinocyte apoptosis and photosensitivity. However, LC ADAM17 activity is reduced in non-lesional lupus model skin, and data point to reduced LC- mediated protection in human lupus. Here, we asked about the role of the IFN-rich lupus skin environment in LC dysfunction and the implications of this regulation for photosensitivity.MethodsGene expression patterns in non-lesional skin from human lupus and multiple murine models were examined. We used MRL/lpr, B6.Sle1yaa, and imiquimod models of lupus in in vivo studies to assess the role of IFN-I in LC ADAM17 dysfunction and photosensitivity.ResultsWe show a shared IFN-rich environment in non-lesional skin across human and murine model systems, that IFN-I inhibits LC ADAM17 activity, and that anti-IFNAR in lupus models restores LC ADAM17 function and reduces photosensitivity in EGFR and LC ADAM17- dependent manners. Reactive oxygen species (ROS) can mediate ADAM17 activity, and we show reduced LC ROS expression in lupus models that is restored by anti-IFNAR.ConclusionsOur findings suggest that IFN-I promotes photosensitivity by causing LC ADAM17 dysfunction and that anifrolumab ameliorates lupus skin disease at least in part by restoring LC function. This work provides insight into IFN-I-mediated disease mechanisms, LC regulation, and a mechanism of action for anifrolumab in lupus.