67 research outputs found

    Comparing and contrasting person-environment fit and misfit

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    For previous Fit e-Conferences, we have presented various aspects of our research on how person-environment (PE) fit and misfit compare. We have argued that because so little is known about how individuals experience fit and misfit at work, qualitative, exploratory research was called for (Talbot &amp; Billsberry, 2007; 2008). Last year, our e-conference contribution detailed how using causal mapping in PE fit research would enable individuals&rsquo; experiences of fit and misfit to be captured and, as well as generating rich idiographic data, would further be amenable to nomothetic analysis (Talbot, Ambrosini &amp; Billsberry, 2009). This paper briefly reviews why we set out to research employees&rsquo; fit and misfit perceptions, how we used causal mapping and discusses the main findings from our research.<br /

    Mapping fit : maximising idiographic and nomothetic benefits

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    In this paper we have argue that collecting data via causal mapping, which allow to capture rich and detailed data about how people make sense of their fit or misfit can allow for both nomothetic and idiographic research, and hence may be a strong base from which to develop our understanding of fit and as such develop our understanding of the fit construct.<br /

    Book review of 'the people make the place: dynamic linkages between individuals and organizations edited by D. Brent Smith'

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    The People Make the Place is a festschrift celebrating the work of industrial/organizational psychologist Benjamin Schneider. It contains 11 specially written chapters each addressing a different element of Schneider’s work. The twelfth chapter, written by the honored scholar, summarizes the contributions and uses the opportunity to clarify many of the ideas surrounding attraction-selection-attrition (ASA) theory

    Vitamin D status, cognitive decline and incident dementia : the Canadian Study of Health and Aging

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    Objective: Vitamin D could prevent cognitive decline because of its neuroprotective, anti-inflammatory and antioxidant properties. This study aimed to evaluate the associations of plasma 25-hydroxyvitamin D (25(OH)D) concentrations with global cognitive function and incident dementia, including Alzheimer’s disease (AD). Methods: The Canadian Study of Health and Aging is a 10-year cohort study of a representative sample of individuals aged 65years or older. A total of 661 subjects initially without dementia with frozen blood samples and follow-up data were included. Global cognitive function was measured using the validated Modified Mini-Mental State (3MS) examination. A consensus diagnosis of all-cause dementia and AD was made between the physician and the neuropsychologist according to published criteria. Cognitive decline for a 5-year increase in age at specific 25(OH)D concentrations was obtained using linear mixedmodels with repeated measures. Hazard ratios of incident dementia and AD were obtained using semi-parametric proportionalhazards models with age as time scale. Results: Over a mean follow-up of 5.4 years, 141 subjects developed dementia of which 100 were AD. Overall, no significant association was found between 25(OH)D and cognitive decline, dementia or AD. Higher 25(OH)D concentrations were associated with an increased risk of dementia and AD in women, but not in men. Conclusion: This study does not support a protective effect of vitamin D status on cognitive function. Further research is needed toclarify the relation by sex.Objectif : La vitamine D pourrait avoir un effet protecteur sur le déclin cognitif en raison de ses propriétés neuroprotectrices, anti-inflammatoires et antioxydantes. L’objectif de cette étude était d’évaluer les associations entre la concentration plasmatique de 25-hydroxyvitamine D (25(OH)D), la fonction cognitive globale et l’incidence de la démence incluant la maladie d’Alzheimer (MA). Méthodes: L’Étude sur la santé et le vieillissement au Canada est une étude de cohorte de 10 ans réalisée dans un échantillon représentatif des Canadiens âgés de 65 ans et plus. Un total de 661 participants sans démence, pour lesquels un échantillon sanguin congelé et des données au suivi étaient disponibles, ont été inclus dans l’analyse. La fonction cognitive globale a été mesurée à l’aide d’un outil validé, le Modified Mini-Mental State(3MS) Examination. Les diagnostics de démence toutes cause set de MA ont été obtenus par consensus entre un médecin généraliste et un neuropsychologue selon des critères publiés. Le déclin cognitif pour chaque augmentation de 5 ans d’âge à des concentrations spécifiques de 25(OH)D a été mesuré à l’aide de modèles linéaires mixtes avec données répétées. Des rapports de risques de la démence et de la MA ont été obtenus à l’aide de modèles à risques proportionnels semi-paramétriques en utilisant l’âge comme échelle du temps. Résultats : En cours de suivi (moyenne : 5,4 ans), 141 individus ont développé une démence dont 100 étaient la MA. Globalement, aucune association statistiquement significative n’a été observée entre le 25(OH)D et le déclin cognitif, la démence ou la MA. Des concentrations plus élevées de 25(OH)D étaient associées à une augmentation du risque de démence et de MA chez les femmes, mais pas chez les hommes. Conclusion : Cette étude n’appuie pas l’hypothèse d’un effet protecteur de la vitamine D sur la fonction cognitive. D’autres études seraient nécessaires pour clarifier la relation selon le sexe

    Misfit: what do you do when you can't be yourself at work?

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    ATAXIN-2 intermediate-length polyglutamine expansions elicit ALS-associated metabolic and immune phenotypes

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    Intermediate-length repeat expansions in ATAXIN-2 (ATXN2) are the strongest genetic risk factor for amyotrophic lateral sclerosis (ALS). At the molecular level, ATXN2 intermediate expansions enhance TDP-43 toxicity and pathology. However, whether this triggers ALS pathogenesis at the cellular and functional level remains unknown. Here, we combine patient-derived and mouse models to dissect the effects of ATXN2 intermediate expansions in an ALS background. iPSC-derived motor neurons from ATXN2-ALS patients show altered stress granules, neurite damage and abnormal electrophysiological properties compared to healthy control and other familial ALS mutations. In TDP-43Tg-ALS mice, ATXN2-Q33 causes reduced motor function, NMJ alterations, neuron degeneration and altered in vitro stress granule dynamics. Furthermore, gene expression changes related to mitochondrial function and inflammatory response are detected and confirmed at the cellular level in mice and human neuron and organoid models. Together, these results define pathogenic defects underlying ATXN2-ALS and provide a framework for future research into ATXN2-dependent pathogenesis and therapy

    A value-based comparison of the management of ambulatory respiratory diseases in walk-in clinics, primary care practices, and emergency departments : protocol for a multicenter prospective cohort study

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    Background: In Canada, 30%-60% of patients presenting to emergency departments are ambulatory. This category has been labeled as a source of emergency department overuse. Acting on the presumption that primary care practices and walk-in clinics offer equivalent care at a lower cost, governments have invested massively in improving access to these alternative settings in the hope that patients would present there instead when possible, thereby reducing the load on emergency departments. Data in support of this approach remain scarce and equivocal. Objective: The aim of this study is to compare the value of care received in emergency departments, walk-in clinics, and primary care practices by ambulatory patients with upper respiratory tract infection, sinusitis, otitis media, tonsillitis, pharyngitis, bronchitis, influenza-like illness, pneumonia, acute asthma, or acute exacerbation of chronic obstructive pulmonary disease. Methods: A multicenter prospective cohort study will be performed in Ontario and Québec. In phase 1, a time-driven activity-based costing method will be applied at each of the 15 study sites. This method uses time as a cost driver to allocate direct costs (eg, medication), consumable expenditures (eg, needles), overhead costs (eg, building maintenance), and physician charges to patient care. Thus, the cost of a care episode will be proportional to the time spent receiving the care. At the end of this phase, a list of care process costs will be generated and used to calculate the cost of each consultation during phase 2, in which a prospective cohort of patients will be monitored to compare the care received in each setting. Patients aged 18 years and older, ambulatory throughout the care episode, and discharged to home with one of the aforementioned targeted diagnoses will be considered. The estimated sample size is 1485 patients. The 3 types of care settings will be compared on the basis of primary outcomes in terms of the proportion of return visits to any site 3 and 7 days after the initial visit and the mean cost of care. The secondary outcomes measured will include scores on patient-reported outcome and experience measures and mean costs borne wholly by patients. We will use multilevel generalized linear models to compare the care settings and an overlap weights approach to adjust for confounding factors related to age, sex, gender, ethnicity, comorbidities, registration with a family physician, socioeconomic status, and severity of illness. Results: Phase 1 will begin in 2021 and phase 2, in 2023. The results will be available in 2025. Conclusions: The end point of our program will be for deciders, patients, and care providers to be able to determine the most appropriate care setting for the management of ambulatory emergency respiratory conditions, based on the quality and cost of care associated with each alternative
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