39 research outputs found
Ownership of co-creation assets: driving B2B value propositions in the service economy
The benefits of specialization have been driving the rise of the service economy and pushing capability frontiers and economic growth. In service economies, almost any activity, asset, and skill can be bought on competitive markets, making it harder to build competitive advantage on any of those inputs. Against that background, the question emerges what constitutes sustainable value propositions of service providers. Drawing on an emerging stream of research on the non-ownership value of services, we argue that service providers create value by taking on ownership of service assets and thereby transform uncertainty of value creation into economic opportunities. In our view, service providers offer the essential value proposition of transforming their clients’ uncertainty downsides into opportunities related to assets such as vehicles, real estate, equipment and computing platforms. Clients benefit by delegating ownership of assets to the domain of a service provider. In turn, clients can focus their investment on their most promising assets. Service providers create sustainable competitive advantage by assuming ownership and excelling at the management of (a) unique physical assets, (b) unique intangible assets and (c) maintaining an appropriate architecture of social capital through customer relationships and business ecosystems
Tides in colliding galaxies
Long tails and streams of stars are the most noticeable upshots of galaxy
collisions. Their origin as gravitational, tidal, disturbances has however been
recognized only less than fifty years ago and more than ten years after their
first observations. This Review describes how the idea of galactic tides
emerged, in particular thanks to the advances in numerical simulations, from
the first ones that included tens of particles to the most sophisticated ones
with tens of millions of them and state-of-the-art hydrodynamical
prescriptions. Theoretical aspects pertaining to the formation of tidal tails
are then presented. The third part of the review turns to observations and
underlines the need for collecting deep multi-wavelength data to tackle the
variety of physical processes exhibited by collisional debris. Tidal tails are
not just stellar structures, but turn out to contain all the components usually
found in galactic disks, in particular atomic / molecular gas and dust. They
host star-forming complexes and are able to form star-clusters or even
second-generation dwarf galaxies. The final part of the review discusses what
tidal tails can tell us (or not) about the structure and content of present-day
galaxies, including their dark components, and explains how tidal tails may be
used to probe the past evolution of galaxies and their mass assembly history.
On-going deep wide-field surveys disclose many new low-surface brightness
structures in the nearby Universe, offering great opportunities for attempting
galactic archeology with tidal tails.Comment: 46 pages, 13 figures, Review to be published in "Tidal effects in
Astronomy and Astrophysics", Lecture Notes in Physics. Comments are most
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Activated p-AKT, but not MDM2, drives malignant progression in <i>Ras/Fos/PTEN<sup>null</sup></i> skin carcinogenesis via p53/p21 loss and elevated cyclin D1/E2 expression
Tumour progression depends on a complex combination of the genetic mutation milieu pitted against the sentinel systems that have evolved to resist carcinogenesis at each specific stage. To investigate tumour progression mechanism in transgenic mouse skin carcinogenesis, inducible PTEN ablation [<i>Δ5PTEN</i>] was introduced into the epidermis of mice expressing activated ras<sup>Ha</sup>/fos oncogenes. RU486-treated HK1.ras/fos-Δ5PTEN mice exhibited accelerated papillomatogenesis but malignant conversion was delayed due to compensatory p53/p21 expression. Following p53 loss malignant progression was limited to well-differentiated squamous cell carcinoma via persistent p21 expression and down regulation of cyclin E2. Analysis of AKT activity during papillomatogenesis showed reduced p-AKT expression, associated with fos/PTEN feedback, which returned following p53 loss to circumvent/antagonise p21 expression; co-operate with MAPK signalling [i.e. elevated ERK1/2 expression]; and accelerate tumour progression via increased cyclin D1 and E2 expression. In contrast elevated, suprabasal MDM2 expression in p53-positive papillomas was lost in parallel to p53 loss; hence sustained MDM2-mediated p53 ubiquination does not appear to influence this progression mechanism. These data suggest p53/p21 counter deregulated MAPK signalling during papillomatogenesis and help minimise consequences of PTEN loss via p-AKT inhibition. Stepwise p53/p21 loss subsequently facilitates ras/MAPK/fos co-operation with PTEN/AKT activities to accelerate malignant progression via major failures in cell cycle control. The interplay between these common mutations thus create unique contexts that have important implications for therapies geared to reactivating p53/p21 functions or that target ras/MAPK/fos and PTEN/AKT signalling pathways