391 research outputs found
Estimated Average Glucose and Self-Monitored Mean Blood Glucose Are Discordant Estimates of Glycemic Control
Peer-to-Peer and Mass Communication Effect on Revolution Dynamics
Revolution dynamics is studied through a minimal Ising model with three main
influences (fields): personal conservatism (power-law distributed),
inter-personal and group pressure, and a global field incorporating
peer-to-peer and mass communications, which is generated bottom-up from the
revolutionary faction. A rich phase diagram appears separating possible
terminal stages of the revolution, characterizing failure phases by the
features of the individuals who had joined the revolution. An exhaustive
solution of the model is produced, allowing predictions to be made on the
revolution's outcome
House price Keynesianism and the contradictions of the modern investor subject
This article conceptualises the marked downturn in UK house prices in the 2007-2009 period in relation to longer-term processes of national economic restructuring centred on a new model of homeownership. The structure of UK house prices has been impacted markedly by the Labour Government‟s efforts to ingrain a particular notion of financial literacy amid the move towards an increasingly asset-based system of welfare. New model welfare recipients and new model homeowners have thereby been co-constituted in a manner consistent with a new UK growth regime of „house price Keynesianism‟. However, the investor subjects who drive such growth are necessarily rendered uncertain as compared with the idealised image of Government policy because of their reliance on the credit-creating decisions of private financial institutions. The recent steep decline in UK house prices is explained here as an epiphenomenon of the disruptive effect on the idealised image caused by the dependence of investor subjects on pricing dynamics not of their making
Cluster Performance reconsidered: Structure, Linkages and Paths in the German Biotechnology Industry, 1996-2003
This paper addresses the evolution of biotechnology clusters in Germany between 1996 and 2003, paying particular attention to their respective composition in terms of venture capital, basic science institutions and biotechnology firms. Drawing upon the significance of co-location of "money and ideas", the literature stressing the importance of a cluster's openness and external linkages, and the path dependency debate, the paper aims to analyse how certain cluster characteristics correspond with its overall performance. After identifying different cluster types, we investigate their internal and external interconnectivity in comparative manner and draw on changes in cluster composition. Our results indicate that the structure, i.e. to which group the cluster belongs, and the openness towards external knowledge flows deliver merely unsystematic indications with regard to a cluster's overall success. Its ability to change composition towards a more balanced ratio of science and capital over time, on the other hand, turns out as a key explanatory factor. Hence, the dynamic perspective proves effective illuminating cluster growth and performance, where our explorative findings provide a promising avenue for further evolutionary research
Crises and collective socio-economic phenomena: simple models and challenges
Financial and economic history is strewn with bubbles and crashes, booms and
busts, crises and upheavals of all sorts. Understanding the origin of these
events is arguably one of the most important problems in economic theory. In
this paper, we review recent efforts to include heterogeneities and
interactions in models of decision. We argue that the Random Field Ising model
(RFIM) indeed provides a unifying framework to account for many collective
socio-economic phenomena that lead to sudden ruptures and crises. We discuss
different models that can capture potentially destabilising self-referential
feedback loops, induced either by herding, i.e. reference to peers, or
trending, i.e. reference to the past, and account for some of the phenomenology
missing in the standard models. We discuss some empirically testable
predictions of these models, for example robust signatures of RFIM-like herding
effects, or the logarithmic decay of spatial correlations of voting patterns.
One of the most striking result, inspired by statistical physics methods, is
that Adam Smith's invisible hand can badly fail at solving simple coordination
problems. We also insist on the issue of time-scales, that can be extremely
long in some cases, and prevent socially optimal equilibria to be reached. As a
theoretical challenge, the study of so-called "detailed-balance" violating
decision rules is needed to decide whether conclusions based on current models
(that all assume detailed-balance) are indeed robust and generic.Comment: Review paper accepted for a special issue of J Stat Phys; several
minor improvements along reviewers' comment
Securitization and financialization
Securitization and financialization are the main causes of the financial crisis. These two concepts explain not only Minsky’s financial instability hypothesis but also the off-balance-sheet operations represented by erivative
products, which are closely related to mortgage loans. Financial intermediaries in need of liquidity did everything in their power so that the securitization of assets could have a life of its own in financial operations. This is a process that is endogenous to the development of financialization. Because said process
was a violation of the monetary economy, it was necessary for central banks to intervene as “lenders of last resort” as well as to nationalize and restructure all the financial intermediaries
Encapsidation of APOBEC3G into HIV-1 virions involves lipid raft association and does not correlate with APOBEC3G oligomerization
<p>Abstract</p> <p>Background</p> <p>The cellular cytidine deaminase APOBEC3G (A3G), when incorporated into the human immunodeficiency virus type 1 (HIV-1), renders viral particles non-infectious. We previously observed that mutation of a single cysteine residue of A3G (C100S) inhibited A3G packaging. In addition, several recent studies showed that mutation of tryptophan 127 (W127) and tyrosine 124 (Y124) inhibited A3G encapsidation suggesting that the N-terminal CDA constitutes a viral packaging signal in A3G. It was also reported that W127 and Y124 affect A3G oligomerization.</p> <p>Results</p> <p>Here we studied the mechanistic basis of the packaging defect of A3G W127A and Y124A mutants. Interestingly, cell fractionation studies revealed a strong correlation between encapsidation, lipid raft association, and genomic RNA binding of A3G. Surprisingly, the presence of a C-terminal epitope tag affected lipid raft association and encapsidation of the A3G W127A mutant but had no effect on wt A3G encapsidation, lipid raft association, and interaction with viral genomic RNA. Mutation of Y124 abolished A3G encapsidation irrespective of the presence or absence of an epitope tag. Contrasting a recent report, our co-immunoprecipitation studies failed to reveal a correlation between A3G oligomerization and A3G encapsidation. In fact, our W127A and Y124A mutants both retained the ability to oligomerize.</p> <p>Conclusion</p> <p>Our results confirm that W127 and Y124 residues in A3G are important for encapsidation into HIV-1 virions and our data establish a novel correlation between genomic RNA binding, lipid raft association, and viral packaging of A3G. In contrast, we were unable to confirm a role of W127 and Y124 in A3G oligomerization and we thus failed to confirm a correlation between A3G oligomerization and virus encapsidation.</p
The cellular source for APOBEC3G's incorporation into HIV-1
<p>Abstract</p> <p>Background</p> <p>Human APOBEC3G (hA3G) has been identified as a cellular inhibitor of HIV-1 infectivity. Viral incorporation of hA3G is an essential step for its antiviral activity. Although the mechanism underlying hA3G virion encapsidation has been investigated extensively, the cellular source of viral hA3G remains unclear.</p> <p>Results</p> <p>Previous studies have shown that hA3G forms low-molecular-mass (LMM) and high-molecular-mass (HMM) complexes. Our work herein provides evidence that the majority of newly-synthesized hA3G interacts with membrane lipid raft domains to form Lipid raft-associated hA3G (RA hA3G), which serve as the precursor of the mature HMM hA3G complex, while a minority of newly-synthesized hA3G remains in the cytoplasm as a soluble LMM form. The distribution of hA3G among the soluble LMM form, the RA LMM form and the mature forms of HMM is regulated by a mechanism involving the N-terminal part of the linker region and the C-terminus of hA3G. Mutagenesis studies reveal a direct correlation between the ability of hA3G to form the RA LMM complex and its viral incorporation.</p> <p>Conclusions</p> <p>Together these data suggest that the Lipid raft-associated LMM A3G complex functions as the cellular source of viral hA3G.</p
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