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Sökning: L773:1045 2699 OR L773:1522 7111

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1.
  • Engström, Tomas, 1950, et al. (författare)
  • Extended Work Cycle Assembly - A crucial learning experience
  • 1994
  • Ingår i: The International journal of human factors in manufacturing. - : Wiley. - 1045-2699 .- 1522-7111. ; 4:3, s. 293-303
  • Tidskriftsartikel (refereegranskat)abstract
    • This paper reports on a crucial learning experience relating to design principles applied in the Volvo Car Corporation final assembly plant in Uddevalla, Sweden. These principles include the concept of holistic learning, specifically through the creation and transformation of complementary, interrelated physical, semantical, and cognitive structures. We report on the learning environment and learning aids, as well as the learning method applied to the assembly of one-quarter of an automobile performed by one single person. Through the application of this learning concept, it proved possible to dramatically reduce the learning time required for long cycle time assembly work, making cycle times of 2 hours or more a practical proposition for full-scale automotive manufacturing today.
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2.
  • Bengtsson, Peter, et al. (författare)
  • Cooperation in Planning of Production and Working Environments Supported by Computer Graphics
  • 1996
  • Ingår i: The International Journal of Human Factors in Manufacturing. - 1045-2699. ; 6:2, s. 101-130
  • Tidskriftsartikel (refereegranskat)abstract
    • A methodology for studying change processes in working life combining computer-aided planning and cooperation in project groups is evaluated. The methodology is applied and studied in a planning workshop with representatives from manufacturing industries—managers, production engineers, supervisors as well as shop floor workers—and from health-and-safety agencies utilizing the methodology for planning of production, layout, and working environment. The results are presented and discussed with respect to cooperation in project groups, outline of proposals, topics of discussion, and pictures as planning tools.
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3.
  • Chen, H.Y., et al. (författare)
  • Dyslipidemia, inflammation, calcification, and adiposity in aortic stenosis: a genome-wide study
  • 2023
  • Ingår i: European Heart Journal. - : Oxford University Press. - 0195-668X .- 1522-9645. ; 44:21, s. 1927-1939
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims Although highly heritable, the genetic etiology of calcific aortic stenosis (AS) remains incompletely understood. The aim of this study was to discover novel genetic contributors to AS and to integrate functional, expression, and cross-phenotype data to identify mechanisms of AS. Methods and results A genome-wide meta-analysis of 11.6 million variants in 10 cohorts involving 653 867 European ancestry participants (13 765 cases) was performed. Seventeen loci were associated with AS at P ≤ 5 × 10−8, of which 15 replicated in an independent cohort of 90 828 participants (7111 cases), including CELSR2–SORT1, NLRP6, and SMC2. A genetic risk score comprised of the index variants was associated with AS [odds ratio (OR) per standard deviation, 1.31; 95% confidence interval (CI), 1.26–1.35; P = 2.7 × 10−51] and aortic valve calcium (OR per standard deviation, 1.22; 95% CI, 1.08–1.37; P = 1.4 × 10−3), after adjustment for known risk factors. A phenome-wide association study indicated multiple associations with coronary artery disease, apolipoprotein B, and triglycerides. Mendelian randomization supported a causal role for apolipoprotein B-containing lipoprotein particles in AS (OR per g/L of apolipoprotein B, 3.85; 95% CI, 2.90–5.12; P = 2.1 × 10−20) and replicated previous findings of causality for lipoprotein(a) (OR per natural logarithm, 1.20; 95% CI, 1.17–1.23; P = 4.8 × 10−73) and body mass index (OR per kg/m2, 1.07; 95% CI, 1.05–1.9; P = 1.9 × 10−12). Colocalization analyses using the GTEx database identified a role for differential expression of the genes LPA, SORT1, ACTR2, NOTCH4, IL6R, and FADS. Conclusion Dyslipidemia, inflammation, calcification, and adiposity play important roles in the etiology of AS, implicating novel treatments and prevention strategies. © The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology.
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