Creating continuing education courses to optimize safety and independence among older adults with low vision

INTRODUCTION: Continuing Education (CE) courses for allied health professionals do not consistently reflect the needs of adult learners and may not result in practice changes. In areas of allied health practice with a strong evidence base, poor quality CE courses stunt the dissemination of information which could improve the quality of life of clients. One such area is improving safety and independence of older adults with low vision, who are at increased risk of falls and functional limitations as a result of their visual impairments. DESCRIPTION OF DOCTORAL CAPSTONE: The aim of this doctoral capstone was to discuss the theory and evidence for the creation of effective, learner-centered CE courses and to apply these findings to the creation of CE courses for allied health professionals on the topic of community-dwelling older adults with low vision. RESULTS: The resulting CE courses were compared to the guidelines for a theory-driven, evidence-based course and were found to adhere to quality standards of: use of a needs assessment, reflection of the real-life context of learners, incorporation of active learning and reflection components, inclusion of visible pedagogy, and evaluation of the translation of learning to practice. CONCLUSION: CE courses that adhere to evidence-based, learner centered methods produce better learning and satisfaction outcomes for participants. CE course creators should adhere to these guidelines and advertise the use of theory and evidence to enable clinician participants to identify high-quality continuing education courses. Clinicians who gain knowledge in the areas of low vision diagnoses, screening, referrals, interventions, and resources, through attendance at a well-designed CE course, will be better able to identify clients with low vision and provide evidence-based care which has been found to improve client safety and independence

Role of host genetic diversity for susceptibility-to-infection in the evolution of virulence of a plant virus

This article has been accepted for publication in Virus Evolution published by Oxford University Press.[EN] Predicting viral emergence is difficult due to the stochastic nature of the underlying processes and the many factors that govern pathogen evolution. Environmental factors affecting the host, the pathogen and the interaction between both are key in emergence. In particular, infectious disease dynamics are affected by spatiotemporal heterogeneity in their environments. A broad knowledge of these factors will allow better estimating where and when viral emergence is more likely to occur. Here, we investigate how the population structure for susceptibility-to-infection genes of the plant Arabidopsis thaliana shapes the evolution of Turnip mosaic virus (TuMV). For doing so we have evolved TuMV lineages in two radically different host population structures: (1) a metapopulation subdivided into six demes (subpopulations); each one being composed of individuals from only one of six possible A. thaliana ecotypes and (2) a well-mixed population constituted by equal number of plants from the same six A. thaliana ecotypes. These two populations were evolved for twelve serial passages. At the end of the experimental evolution, we found faster adaptation of TuMV to each ecotype in the metapopulation than in the well-mixed heterogeneous host populations. However, viruses evolved in well-mixed populations were more pathogenic and infectious than viruses evolved in the metapopulation. Furthermore, the viruses evolved in the demes showed stronger signatures of local specialization than viruses evolved in the well-mixed populations. These results illustrate how the genetic diversity of hosts in an experimental ecosystem favors the evolution of virulence of a pathogen.We thank Francisca de la Iglesia for continuous excellent technical support. Work was supported by Spain's Agencia Estatal de Investigacion-FEDER grant BFU2015-65037-P and Generalitat Valenciana grant GRISOLIA/2018/005 to S.F.E. R.G. was supported by Spain's Agencia Estatal de Investigacion pre-doctoral contract BES-2016-077078.González, R.; Butkovic, A.; Elena Fito, SF. (2019). Role of host genetic diversity for susceptibility-to-infection in the evolution of virulence of a plant virus. Virus Evolution. 5(2):1-12. https://doi.org/10.1093/ve/vez024S11252Altizer, S., Dobson, A., Hosseini, P., Hudson, P., Pascual, M., & Rohani, P. (2006). Seasonality and the dynamics of infectious diseases. Ecology Letters, 9(4), 467-484. doi:10.1111/j.1461-0248.2005.00879.xAnttila, J., Kaitala, V., Laakso, J., & Ruokolainen, L. (2015). 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How can the MHC mediate social odor via the microbiota community? A deep dive into mechanisms

Genes of the major histocompatibility complex (MHC) have long been linked to odor signaling and recently researchers’ attention has focused on MHC structuring of microbial communities and how this may in turn impact odor. However, understanding of the mechanisms through which the MHC could affect the microbiota to produce a chemical signal that is both reliable and strong enough to ensure unambiguous transmission of behaviorally important information remains poor. This is largely because empirical studies are rare, predictions are unclear, and the underlying immunological mechanisms governing MHC-microbiota interactions are often neglected. Here we review the immunological processes involving MHC class II (MHC-II) that could affect the commensal community. Focusing on immunological and medical research, we provide background knowledge for non-immunologists by describing key players within the vertebrate immune system relating to MHC-II molecules (which present extracellular-derived peptides, and thus interact with extracellular commensal microbes). We then systematically review the literature investigating MHC-odor-microbiota interactions in animals and identify areas for future research. These insights will help to design studies that are able to explore the role of MHC-II and the microbiota in the behavior of wild populations in their natural environment and consequently propel this research area forward

Absence of MHC class II on cDCs results in microbial-dependent intestinal inflammation.

Conventional dendritic cells (cDCs) play an essential role in host immunity by initiating adaptive T cell responses and by serving as innate immune sensors. Although both innate and adaptive functions of cDCs are well documented, their relative importance in maintaining immune homeostasis is poorly understood. To examine the significance of cDC-initiated adaptive immunity in maintaining homeostasis, independent of their innate activities, we generated a cDC-specific Cre mouse and crossed it to a floxed MHC class II (MHCII) mouse. Absence of MHCII on cDCs resulted in chronic intestinal inflammation that was alleviated by antibiotic treatment and entirely averted under germ-free conditions. Uncoupling innate and adaptive functions of cDCs revealed that innate immune functions of cDCs are insufficient to maintain homeostasis and antigen presentation by cDCs is essential for a mutualistic relationship between the host and intestinal bacteria

What has GWAS done for HLA and disease associations?

The major histocompatibility complex (MHC) is located in chromosome 6p21 and contains crucial regulators of immune response, including human leucocyte antigen (HLA) genes, alongside other genes with nonimmunological roles. More recently, a repertoire of noncoding RNA genes, including expressed pseudogenes, has also been identified. The MHC is the most gene dense and most polymorphic part of the human genome. The region exhibits haplotype-specific linkage disequilibrium patterns, contains the strongest cis- and trans-eQTLs/meQTLs in the genome and is known as a hot spot for disease associations. Another layer of complexity is provided to the region by the extreme structural variation and copy number variations. While the HLA-B gene has the highest number of alleles, the HLA-DR/DQ subregion is structurally most variable and shows the highest number of disease associations. Reliance on a single reference sequence has complicated the design, execution and analysis of GWAS for the MHC region and not infrequently, the MHC region has even been excluded from the analysis of GWAS data. Here, we contrast features of the MHC region with the rest of the genome and highlight its complexities, including its functional polymorphisms beyond those determined by single nucleotide polymorphisms or single amino acid residues. One of the several issues with customary GWAS analysis is that it does not address this additional layer of polymorphisms unique to the MHC region. We highlight alternative approaches that may assist with the analysis of GWAS data from the MHC region and unravel associations with all functional polymorphisms beyond single SNPs. We suggest that despite already showing the highest number of disease associations, the true extent of the involvement of the MHC region in disease genetics may not have been uncovered

Regionalized Development and Maintenance of the Intestinal Adaptive Immune Landscape

The intestinal immune system has the daunting task of protecting us from pathogenic insults while limiting inflammatory responses against the resident commensal microbiota and providing tolerance to food antigens. This role is particularly impressive when one considers the vast mucosal surface and changing landscape that the intestinal immune system must monitor. In this review, we highlight regional differences in the development and composition of the adaptive immune landscape of the intestine and the impact of local intrinsic and environmental factors that shape this process. To conclude, we review the evidence for a critical window of opportunity for early-life exposures that affect immune development and alter disease susceptibility later in life