1,725 research outputs found

    When “embedded” means “stuck” : moderating effects of job embeddedness in adverse work environments

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    Job embeddedness is predominately assumed to benefit employees, work groups, and organizations (e.g., higher performance, social cohesion, and lower voluntary turnover). Challenging this assumption, we examined the potentially negative outcomes that may occur if employees are embedded in an adverse work environment - feeling “stuck”, yet unable to exit a negative situation. More specifically, we considered two factors representing adverse work conditions: abusive supervision and job insecurity. Drawing from conservation-of-resources theory, we hypothesized that job embeddedness would moderate the relationship between these conditions and outcomes of voluntary turnover, physical health, emotional exhaustion, and sleep quality/quantity, such that employees embedded in more adverse environments would be less likely to quit, but would experience more negative personal outcomes. Results from two independent samples, one in Japan (N=597) and one in the United States (N=283), provide support for the hypothesized pattern of interaction effects, thereby highlighting a largely neglected “dark side” of job embeddedness

    Wildbook: Crowdsourcing, computer vision, and data science for conservation

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    Photographs, taken by field scientists, tourists, automated cameras, and incidental photographers, are the most abundant source of data on wildlife today. Wildbook is an autonomous computational system that starts from massive collections of images and, by detecting various species of animals and identifying individuals, combined with sophisticated data management, turns them into high resolution information database, enabling scientific inquiry, conservation, and citizen science. We have built Wildbooks for whales (flukebook.org), sharks (whaleshark.org), two species of zebras (Grevy's and plains), and several others. In January 2016, Wildbook enabled the first ever full species (the endangered Grevy's zebra) census using photographs taken by ordinary citizens in Kenya. The resulting numbers are now the official species census used by IUCN Red List: http://www.iucnredlist.org/details/7950/0. In 2016, Wildbook partnered up with WWF to build Wildbook for Sea Turtles, Internet of Turtles (IoT), as well as systems for seals and lynx. Most recently, we have demonstrated that we can now use publicly available social media images to count and track wild animals. In this paper we present and discuss both the impact and challenges that the use of crowdsourced images can have on wildlife conservation.Comment: Presented at the Data For Good Exchange 201

    Comparing strategies for United States veterans' mortality ascertainment

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    BACKGROUND: We aimed to determine optimal strategies for complete mortality ascertainment comparing death certificates and United States (US) Veterans Administration (VA) records. METHODS: We constructed a cohort of California veterans who died in fiscal year (FY) 2000 and used VA services the year before death. We determined decedent status using California death certificates linked to VA utilization data and the VA Beneficiary Identification and Records Locator System (BIRLS) death file. We compared the characteristics of decedents who would not have been identified by either single source (e.g., VA BIRLS alone or California death certificates alone) with the rest of the cohort. RESULTS: A total of 8,813 veteran decedents were identified from both VA decedent files and death certificates. Of all decedents, 5,698 / 8,813 (65%) veterans were identified in both source files, but 2,426 / 8,813 (28%) decedents were not identified in VA BIRLS, and 689 / 8,813 (8%) were not identified in death certificates. Compared to the rest of the cohort, decedents whose mortality status was ascertained through either single source differed by race / ethnicity, marital status, and California residence. Clinically, veterans identified from either single source had less comorbidity and were less likely to have been users of VA inpatient or long term care, but equally or more likely to have been users of VA outpatient services. CONCLUSION: As single sources, VA decedent files and death certificates each provided an incomplete record, and death ascertainment was improved by using both source files. Potential bias may vary depending on analytic interest

    IL-17A induces Pendrin expression and chloride-bicarbonate exchange in human bronchial epithelial cells

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    The epithelium plays an active role in the response to inhaled pathogens in part by responding to signals from the immune system. Epithelial responses may include changes in chemokine expression, increased mucin production and antimicrobial peptide secretion, and changes in ion transport. We previously demonstrated that interleukin-17A (IL-17A), which is critical for lung host defense against extracellular bacteria, significantly raised airway surface pH in vitro, a finding that is common to a number of inflammatory diseases. Using microarray analysis of normal human bronchial epithelial (HBE) cells treated with IL-17A, we identified the electroneutral chloride-bicarbonate exchanger Pendrin (SLC26A4) as a potential mediator of this effect. These data were verified by real-time, quantitative PCR that demonstrated a time-dependent increase in Pendrin mRNA expression in HBE cells treated with IL-17A up to 48 h. Using immunoblotting and immunofluorescence, we confirmed that Pendrin protein expression is increased in IL-17 treated HBE cells and that it is primarily localized to the mucosal surface of the cells. Functional studies using live-cell fluorescence to measure intracellular pH demonstrated that IL-17A induced chloride-bicarbonate exchange in HBE cells that was not present in the absence of IL-17A. Furthermore, HBE cells treated with short interfering RNA against Pendrin showed substantially reduced chloride-bicarbonate exchange. These data suggest that Pendrin is part of IL-17A-dependent epithelial changes and that Pendrin may therefore be a therapeutic target in IL-17A-dependent lung disease. © 2014 Adams et al
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