PURPOSE: The main objective of this study was to determine the relationship between quality of life, social functioning, depressive symptoms, self-efficacy, physical function, and socioeconomic status (SES) in community-dwelling older adults.METHODS: A cross-sectional design was used to examine the relationships. A sample of 193 community-dwelling older adults completed the measurements. Structural equation modeling with full information maximum likelihood in LISREL was used to evaluate the relationships between the latent variables (SES, social functioning, depressive symptoms, self-efficacy, physical function, and quality of life).RESULTS: The path analysis exhibited significant effects of SES on physical function, social functioning, depressive symptoms, and self-efficacy (γ = 0.42-0.73), and significant effects in regard to social functioning, depressive symptoms, and self-efficacy on quality of life (γ = 0.27-0.61). There was no direct effect of SES on the quality of life. The model fit indices demonstrated a reasonable fit (χ (2) = 98.3, df = 48, p < 0.001), matching the relative Chi-square criterion and the RMSEA criterion. The model explained 55.5 % of the variance of quality of life.CONCLUSIONS: The path analysis indicated an indirect effect of SES on the quality of life by social functioning, depressive symptoms, and self-efficacy in community-dwelling older adults. Physical function did not have a direct effect on the quality of life. To improve the quality of life in older adults, additional focus is required on the socioeconomic psychosocial differences in the community-dwelling older population.
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In this study, we address the function of role models for entrepreneurship students. By using entrepreneurs as role models, students can get a better and realistic picture of the complexity of the entrepreneurial path. Choosing whom to interview as role model can be diverse, but it can be problematic if, as a result of that choice, the learning effect in the same group of students is different.
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Author supplied: In a production environment where different products are being made in parallel, the path planning for every product can be different. The model proposed in this paper is based on a production environment where the production machines are placed in a grid. A software entity, called product agent, is responsible for the manufacturing of a single product. The product agent will plan a path along the production machines needed for that specific product. In this paper, an optimization is proposed that will reduce the amount of transport between the production machines. The effect of two factors that influence the possibilities for reductions is shown in a simulation, using the proposed optimization scheme. These two factors are the redundancy of production steps in the grid and the
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Huntington’s disease (HD) and various spinocerebellar ataxias (SCA) are autosomal dominantly inherited neurodegenerative disorders caused by a CAG repeat expansion in the disease-related gene1. The impact of HD and SCA on families and individuals is enormous and far reaching, as patients typically display first symptoms during midlife. HD is characterized by unwanted choreatic movements, behavioral and psychiatric disturbances and dementia. SCAs are mainly characterized by ataxia but also other symptoms including cognitive deficits, similarly affecting quality of life and leading to disability. These problems worsen as the disease progresses and affected individuals are no longer able to work, drive, or care for themselves. It places an enormous burden on their family and caregivers, and patients will require intensive nursing home care when disease progresses, and lifespan is reduced. Although the clinical and pathological phenotypes are distinct for each CAG repeat expansion disorder, it is thought that similar molecular mechanisms underlie the effect of expanded CAG repeats in different genes. The predicted Age of Onset (AO) for both HD, SCA1 and SCA3 (and 5 other CAG-repeat diseases) is based on the polyQ expansion, but the CAG/polyQ determines the AO only for 50% (see figure below). A large variety on AO is observed, especially for the most common range between 40 and 50 repeats11,12. Large differences in onset, especially in the range 40-50 CAGs not only imply that current individual predictions for AO are imprecise (affecting important life decisions that patients need to make and also hampering assessment of potential onset-delaying intervention) but also do offer optimism that (patient-related) factors exist that can delay the onset of disease.To address both items, we need to generate a better model, based on patient-derived cells that generates parameters that not only mirror the CAG-repeat length dependency of these diseases, but that also better predicts inter-patient variations in disease susceptibility and effectiveness of interventions. Hereto, we will use a staggered project design as explained in 5.1, in which we first will determine which cellular and molecular determinants (referred to as landscapes) in isogenic iPSC models are associated with increased CAG repeat lengths using deep-learning algorithms (DLA) (WP1). Hereto, we will use a well characterized control cell line in which we modify the CAG repeat length in the endogenous ataxin-1, Ataxin-3 and Huntingtin gene from wildtype Q repeats to intermediate to adult onset and juvenile polyQ repeats. We will next expand the model with cells from the 3 (SCA1, SCA3, and HD) existing and new cohorts of early-onset, adult-onset and late-onset/intermediate repeat patients for which, besides accurate AO information, also clinical parameters (MRI scans, liquor markers etc) will be (made) available. This will be used for validation and to fine-tune the molecular landscapes (again using DLA) towards the best prediction of individual patient related clinical markers and AO (WP3). The same models and (most relevant) landscapes will also be used for evaluations of novel mutant protein lowering strategies as will emerge from WP4.This overall development process of landscape prediction is an iterative process that involves (a) data processing (WP5) (b) unsupervised data exploration and dimensionality reduction to find patterns in data and create “labels” for similarity and (c) development of data supervised Deep Learning (DL) models for landscape prediction based on the labels from previous step. Each iteration starts with data that is generated and deployed according to FAIR principles, and the developed deep learning system will be instrumental to connect these WPs. Insights in algorithm sensitivity from the predictive models will form the basis for discussion with field experts on the distinction and phenotypic consequences. While full development of accurate diagnostics might go beyond the timespan of the 5 year project, ideally our final landscapes can be used for new genetic counselling: when somebody is positive for the gene, can we use his/her cells, feed it into the generated cell-based model and better predict the AO and severity? While this will answer questions from clinicians and patient communities, it will also generate new ones, which is why we will study the ethical implications of such improved diagnostics in advance (WP6).
