7 research outputs found

    Criteria and Guidelines for Human-Centered Work Design in a Digitally Transformed World of Work: Findings from a Formal Consensus Process

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    With the increasing digital transformation, work tasks are changing—in some cases, significantly. Our study addresses the question of whether the established criteria for work design are still sufficient or if they should get updated and additional criteria become necessary in the context of digitalization. In a multistage consensus process involving interdisciplinary groups of experts, we have identified specific criteria for the humane design of work in a world increasingly permeated by digitalized work tools. Starting with an expert workshop using a combined nominal group/focus group technique, followed by a real-time Delphi study, a content analysis and a five-stage peer comment process, we detected 13 criteria and 38 design guidelines for human-centered work in digital transformation. Mapping these with established criteria, it became apparent that some established criteria have experienced a new dynamic because of the digital transformation. For other criteria, a need for digitization-sensitive design is discernible. In addition, criteria have emerged whose necessity is rooted in the digital transformation. A diffusion and stronger interconnection of the various levels of the work system in connection with the digital transformation of work is apparent

    Task2 potassium channels set central respiratory CO2 and O2 sensitivity

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    Task2 K+ channel expression in the central nervous system is surprisingly restricted to a few brainstem nuclei, including the retrotrapezoid (RTN) region. All Task2-positive RTN neurons were lost in mice bearing a Phox2b mutation that causes the human congenital central hypoventilation syndrome. In plethysmography, Task2−/− mice showed disturbed chemosensory function with hypersensitivity to low CO2 concentrations, leading to hyperventilation. Task2 probably is needed to stabilize the membrane potential of chemoreceptive cells. In addition, Task2−/− mice lost the long-term hypoxia-induced respiratory decrease whereas the acute carotid-body-mediated increase was maintained. The lack of anoxia-induced respiratory depression in the isolated brainstem–spinal cord preparation suggested a central origin of the phenotype. Task2 activation by reactive oxygen species generated during hypoxia could silence RTN neurons, thus contributing to respiratory depression. These data identify Task2 as a determinant of central O2 chemoreception and demonstrate that this phenomenon is due to the activity of a small number of neurons located at the ventral medullary surface
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