Despite the central role of legitimacy in social and organizational life, we know little of the subtle meaning-making processes through which organizational phenomena, such as industrial restructuring, are legitimated in contemporary society. Therefore, this paper examines the discursive legitimation strategies used when making sense of global industrial restructuring in the media. Based on a critical discourse analysis of extensive media coverage of a revolutionary pulp and paper sector merger, we distinguish and analyze five legitimation strategies: (1) normalization, (2) authorization, (3) rationalization, (4) moralization, and (5) narrativization. We argue that while these specific legitimation strategies appear in individual texts, their recurring use in the intertextual totality of the public discussion establishes the core elements of the emerging legitimating discourse.Key words: legitimation, discourse, media, industrial restructuring, globalization ‗Legitimacy' and ‗legitimation' play a central role in social action in general and organizational action in particular. In organization studies, legitimacy has been an important theme in several streams of research, but explicit analyses of legitimation are still scarce (e.g. Hybels 1995; Suchman 1995). We argue, in this paper, that there is a specific lack of knowledge concerning the discursive processes, practices, and strategies used to (re)construct senses of legitimacy/illegitimacy. Nevertheless, such knowledge is needed if we want to better understand the complex, but often subtle meaning-making processes through which organizational phenomena, such as industrial restructuring, are legitimated in contemporary society.As a step in this direction, we concentrate in this paper on the discursive legitimation in the media. By adopting a critical discourse analysis (henceforth CDA) perspective and by drawing on previous work by linguists on legitimation (Van Leeuwen and Wodak 1999), we focus on discursive legitimation concerning industrial restructuring. Our aim is to develop an empirically grounded model that will serve organization scholars in trying to understand the micro-level discursive strategies used in legitimating contemporary organizational phenomena. We focus on the media as an 3 important but still not very well-known legitimating arena for organizational phenomena.Our research question is the following: Authors nameWhat are the discursive strategies used when legitimating industrial restructuring in the media?We are consequently not looking at whether specific changes at particular points of time are seen as legitimate by any stakeholder group. Instead, we focus on the subtle discursive strategies that tend to construct a sense of legitimacy around these phenomena in the public discourse.In our analysis, we focus on a ‗revolutionary' Finnish-Swedish merger that paved the way for a series of cross-border mergers and acquisitions, fundamentally changing the international paper and pulp industry. This case created a lively debate in the F...

corporate responsibility, corporate social responsibility, financial performance, corporate social performance,

CD73/ecto-5 0 -nucleotidase dephosphorylates extracellular AMP into adenosine, and it is a key enzyme in the regulation of adenosinergic signaling. The contribution of host CD73 to tumor growth and anti-tumor immunity has not been studied. Here, we show that under physiological conditions CD73-deficient mice had significantly elevated ATPase and ADPase activities in LN T cells. In a melanoma model, the growth of primary tumors and formation of metastasis were significantly attenuated in mice lacking CD73. Among tumor-infiltrating leukocytes there were fewer Tregs and mannose receptor-positive macrophages, and increased IFN-c and NOS2 mRNA production in CD73-deficient mice. Treatment of tumorbearing animals with soluble apyrase, an enzyme hydrolyzing ATP and ADP, significantly inhibited tumor growth and accumulation of intratumoral Tregs and mannose receptorpositive macrophages in the WT C57BL/6 mice but not in the CD73-deficient mice. Pharmacological inhibition of CD73 with a,b-methylene-adenosine-5 0 -diphosphate in WT mice retarded tumor progression similarly to the genetic deletion of CD73. Together these data show that increased pericellular ATP degradation in the absence of CD73 activity in the host cells is a novel mechanism controlling anti-tumor immunity and tumor progression, and that the purinergic balance can be manipulated therapeutically to inhibit tumor growth.

Macrophages are key regulators of fibrosis development and resolution. Elucidating the mechanisms by which they mediate this process is crucial for establishing their therapeutic potential. Here, we use experimental models of liver fibrosis to show that deficiency of the scavenger receptor, stabilin-1, exacerbates fibrosis and delays resolution during the recovery phase. We detected a subset of stabilin-1 + macrophages that were induced at sites of cellular injury close to the hepatic scar in mouse models of liver fibrosis and in human liver disease. Stabilin-1 deficiency abrogated malondialdehyde-LDL (MDA-LDL) uptake by hepatic macrophages and was associated with excess collagen III deposition. Mechanistically, the lack of stabilin-1 led to elevated intrahepatic levels of the profibrogenic chemokine CCL3 and an increase in GFAP + fibrogenic cells. Stabilin-1 −/− macrophages demonstrated a proinflammatory phenotype during liver injury and the normal induction of Ly6C lo monocytes during resolution was absent in stabilin-1 knockouts leading to persistence of fibrosis. Human stabilin-1 + monocytes efficiently internalized MDA-LDL and this suppressed their ability to secrete CCL3, suggesting that loss of stabilin-1 removes a brake to CCL3 secretion. Experiments with cell-lineage-specific knockouts revealed that stabilin-1 expression in myeloid cells is required for the induction of this subset of macrophages and that increased fibrosis occurs in their absence. This study demonstrates a previously unidentified regulatory pathway in fibrogenesis in which a macrophage scavenger receptor protects against organ fibrosis by removing fibrogenic products of lipid peroxidation. Thus, stabilin-1 + macrophages shape the tissue microenvironment during liver injury and healing.stabilin-1 | liver | fibrosis | macrophages | CCL3