41 research outputs found

    Elevating design in the organization

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    Following evidence of its positive contribution to innovation and company performance, many firms are seeking to elevate design to a strategic level. However, little is known as to how this can be achieved. This study draws on the literatures concerned with elevating organizational functions and with organizational legitimacy, and aims to unravel and detail critical practices and potential tensions influencing the elevation of design’s status in firms. To do so, 53 in-depth interviews were undertaken with key informants, representing a range of functional specialisms, in 12 companies, including large multinational companies as well as SMEs. Findings show how six practices – top management support, leadership of the design function, generating awareness of design’s role and contribution, inter-functional coordination, evaluation of design, and formalization of product and service development processes – affect the design elevation process. In contrast with previous studies on raising the status of organizational functions, this research reveals that the same practive can play both positive and negative roles, and that there are fundamental tensions, which should be reconciled if design’s status is to be elevated. Drawing on the concept of organizational legitimacy, we also examine how design moves beyond being seen as pragmatically useful, to being identified as a relevant, alternative way of operating, to being regarded as essential for success. The article concludes by articulating contributions to design and innovation management theory and practice, and to the body of scholarly work seeking to understand how to elevate the status of a function

    The impact of corporate volunteering on CSR image: a consumer perspective

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    Received: 29 June 2013 / Accepted: 15 January 2014Abstract Corporate volunteering (CV) is known to be an effective employee engagement initiative. However, despite the prominence of corporate social responsibility (CSR) in academia and practice, research is yet to investigate whether and how CV may influence consumer perceptions of CSR image and subsequent consumer behaviour. Data collected using an online survey in Australia show perceived familiarity with a company’s CV programme to positively impact CSR image and firm image, partially mediated by others-centred attributions. CSR image, in turn, strengthens affective and cognitive loyalty as well as word-of-mouth. Further analysis reveals the moderating effect of perceived leveraging of the corporate volunteering programme, customer status and the value individuals place on CSR. The paper concludes with theoretical and managerial implications, as well as an agenda for future research.Carolin Plewa, Jodie Conduit, Pascale G. Quester, Claire Johnso

    Polysemic Scaffolding: Explicating Discursive Clashes in Chappelle’s Show

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    This article explicates the discursive foundations that bubble up multiple meanings in racial humor, describing three prominent discursive clashes at the heart of Chappelle’s Show’s polysemic comedy: Egregious stereotyping versus subtler mediated racism, inverted racial stereotypes versus traditional stereotypes, and serious versus nonserious discourse. Throughout the article, I make a case for ‘‘polysemic scaffolding,’’ a method that positions polysemy as a taken-for-granted interaction among text, author, and audience, and instead seeks to understand the discursive patterns that will eventually have their polysemic meanings activated. This article underscores the importance of not only undertaking polysemic criticism, but also of uncovering the discursive scaffolding upon which the polysemy is based

    Murine cytomegalovirus infection exacerbates complex IV deficiency in a model of mitochondrial disease

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    The influence of environmental insults on the onset and progression of mitochondrial diseases is unknown. To evaluate the effects of infection on mitochondrial disease we used a mouse model of Leigh Syndrome, where a missense mutation in the Taco1 gene results in the loss of the translation activator of cytochrome c oxidase subunit I (TACO1) protein. The mutation leads to an isolated complex IV deficiency that mimics the disease pathology observed in human patients with TACO1 mutations. We infected Taco1 mutant and wild-type mice with a murine cytomegalovirus and show that a common viral infection exacerbates the complex IV deficiency in a tissue-specific manner. We identified changes in neuromuscular morphology and tissue-specific regulation of the mammalian target of rapamycin pathway in response to viral infection. Taken together, we report for the first time that a common stress condition, such as viral infection, can exacerbate mitochondrial dysfunction in a genetic model of mitochondrial disease

    Mutation in MRPS34 Compromises Protein Synthesis and Causes Mitochondrial Dysfunction

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    <div><p>The evolutionary divergence of mitochondrial ribosomes from their bacterial and cytoplasmic ancestors has resulted in reduced RNA content and the acquisition of mitochondria-specific proteins. The mitochondrial ribosomal protein of the small subunit 34 (MRPS34) is a mitochondria-specific ribosomal protein found only in chordates, whose function we investigated in mice carrying a homozygous mutation in the nuclear gene encoding this protein. The <i>Mrps34</i> mutation causes a significant decrease of this protein, which we show is required for the stability of the 12S rRNA, the small ribosomal subunit and actively translating ribosomes. The synthesis of all 13 mitochondrially-encoded polypeptides is compromised in the mutant mice, resulting in reduced levels of mitochondrial proteins and complexes, which leads to decreased oxygen consumption and respiratory complex activity. The <i>Mrps34</i> mutation causes tissue-specific molecular changes that result in heterogeneous pathology involving alterations in fractional shortening of the heart and pronounced liver dysfunction that is exacerbated with age. The defects in mitochondrial protein synthesis in the mutant mice are caused by destabilization of the small ribosomal subunit that affects the stability of the mitochondrial ribosome with age.</p></div
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