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Träfflista för sökning "WFRF:(Vahlne G) "

Search: WFRF:(Vahlne G)

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1.
  • Ivarsson, Inge, 1954, et al. (author)
  • Global technology development by colocating R&D and manufacturing: The Case of Swedish manufacturing MNEs
  • 2017
  • In: Industrial and Corporate Change. - : Oxford University Press (OUP). - 0960-6491 .- 1464-3650. ; 26:1, s. 149-168
  • Journal article (peer-reviewed)abstract
    • In this study we analyze the role of colocation between research and development (R&D) and manufacturing for global technology development by multinational enterprises (MNEs). The extant literature suggests that the main strategic role of colocated R&D units is to locally adapt existing products and processes. However, data from 146 foreign R&D units of Sweden’s 17 largest manufacturing MNEs in 2013 show that they instead mainly develop new technology, not only for the local and regional markets, but to a large extent for the global market. A likely explanation is that colocation positively contributes to joint problem-solving and transfer of tacit knowledge between production and R&D personnel, all of which is necessary in new product development, especially in industries characterized by complex products and systems and rapid technological change. A theoretical implication is that depending on industry characteristics, internal cross-functional linkages between R&D and manufacturing can be more critical than external supply- and demand-side factors when it comes to influence where R&D units are located globally.
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2.
  • Johansson, S, et al. (author)
  • Natural killer cell education in mice with single or multiple major histocompatibility complex class I molecules
  • 2005
  • In: The Journal of experimental medicine. - : Rockefeller University Press. - 0022-1007 .- 1540-9538. ; 201:7, s. 1145-1155
  • Journal article (peer-reviewed)abstract
    • The ability of murine NK cells to reject cells lacking self MHC class I expression results from an in vivo education process. To study the impact of individual MHC class I alleles on this process, we generated mice expressing single MHC class I alleles (Kb, Db, Dd, or Ld) or combinations of two or more alleles. All single MHC class I mice rejected MHC class I–deficient cells in an NK cell–dependent way. Expression of Kb or Dd conveyed strong rejection of MHC class I–deficient cells, whereas the expression of Db or Ld resulted in weaker responses. The educating impact of weak ligands (Db and Ld) was further attenuated by the introduction of additional MHC class I alleles, whereas strong ligands (Kb and Dd) maintained their educating impact under such conditions. An analysis of activating and inhibitory receptors in single MHC class I mice suggested that the educating impact of a given MHC class I molecule was controlled both by the number of NK cells affected and by the strength of each MHC class I–Ly49 receptor interaction, indicating that NK cell education may be regulated by a combination of qualitative and quantitative events.
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3.
  • King, Carina, et al. (author)
  • COVID-19—a very visible pandemic
  • 2020
  • In: The Lancet. - : Elsevier. - 0140-6736 .- 1474-547X. ; 396:10248, s. 15-15
  • Journal article (peer-reviewed)
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4.
  • Larsson, P A, et al. (author)
  • Non-random chromosome rearrangements in herpes simplex virus type 1 transformed diploid CHEF cells
  • 1992
  • In: Anticancer Research. - 0250-7005 .- 1791-7530. ; 12:3, s. 863-868
  • Journal article (peer-reviewed)abstract
    • The effects of Herpes simplex virus type 1 (HSV-1) on diploid, non-tumourigenic Chinese hamster embryo fibroblasts (CHEF/18-1D-3) were studied. Six independent lines transformed by HSV-1 alone or by HSV-1 in combination with acyclovir or aqueous tobacco extract were isolated. In contrast to uninfected CHEF/18-1D-3 cells, all transformants grew in soft agar and were tumourigenic in nude mice. Neither infectious virus nor viral antigens could be detected in any of the lines. Cytogenetic analysis revealed clonal chromosome abnormalities in all lines including trisomy for the long arm of chromosome 3 in five lines. In three of these the extra 3q was translocated onto 6p. All lines showed loss of the corresponding 3p arm. The remaining line had a hypodiploid stemline with loss of one chromosome 7. This line also showed a pronounced chromosomal instability with a multitude of mainly sporadic rearrangements. These results show that HSV-1 induced transformation and tumourigenesis in CHEF cells is associated with the induction of chromosome rearrangements, in particular trisomy for 3q.
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7.
  • Magnusson, Yvonne, 1957, et al. (author)
  • Mapping of a functional autoimmune epitope on the beta 1-adrenergic receptor in patients with idiopathic dilated cardiomyopathy.
  • 1990
  • In: The Journal of clinical investigation. - 0021-9738. ; 86:5, s. 1658-63
  • Journal article (peer-reviewed)abstract
    • The presence and properties of serum autoantibodies against beta-adrenergic receptors in patients with idiopathic dilated cardiomyopathy were studied using synthetic peptides derived from the predicted sequences of the human beta-adrenergic receptors. Peptides corresponding to the sequences of the second extracellular loop of the human beta 1- and beta 2-adrenergic receptors were used as antigens in an enzyme immunoassay to screen sera from patients with dilated cardiomyopathy (n = 42), ischemic heart disease (n = 17), or healthy blood donors (n = 34). The sera of thirteen dilated cardiomyopathy patients, none of the ischemic heart disease patients, and four of the healthy controls monospecifically recognized the beta 1-peptide. Only affinity-purified antibodies of these patients had a inhibitory effect on radioligand binding to the beta 1 receptor of C6 rat glioma cells. They recognized the receptor protein by immunoblot and bound in situ to human myocardial tissue. We conclude that a subgroup of patients with idiopathic dilated cardiomyopathy have in their sera autoantibodies specifically directed against the second extracellular loop of the beta 1-adrenergic receptor. These antibodies could serve as a marker of an autoimmune response with physiological and/or pathological implications.
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