Material Futures:Design-led Approaches to Crafting Conversations in the Circular Economy

This paper explores the work in the area of Material Futures – undertaken by researchers at The Glasgow School of Art (GSA). We begin by presenting current debates within the textile sector and outline the challenges of the circular economy. The Scottish Government have established a £17 million fund to catalyse innovative approaches for the circular economy, which support closed-loop systems including collaboration, evaluation of different methods and future material ecologies. We discuss future material ecologies in two case studies in order to extrapolate the ways in which creative and participatory design approaches can be used to stimulate dialogue around the circular economy, broader environmental and economic issues and the socio-cultural implications. We identify six design principles for researchers and practitioners to consider when facilitating circular conversations and the evolving role of the textile designer. We go on to highlight the significance of design-led approaches in strengthening communication, promoting creative action and embedding collaborative ways of working. We conclude by making recommendations for future research and practice and how the insights might be expanded upon to support ethical, responsible and sustainable material futures

Tapping Spin Glasses

We consider a tapping dynamics, analogous to that in experiments on granular media, on spin glasses and ferromagnets on random thin graphs. Between taps, zero temperature single spin flip dynamics takes the system to a metastable state. Tapping, corresponds to flipping simultaneously any spin with probability $p$. This dynamics leads to a stationary regime with a steady state energy $E(p)$. We analytically solve this dynamics for the one dimensional ferromagnet and $\pm J$ spin glass. Numerical simulations for spin glasses and ferromagnets of higher connectivity are carried out, in particular we find a novel first order transition for the ferromagnetic systems.Comment: 5 pages, 3 figures, RevTe

Steady State Behavior of Mechanically Perturbed Spin Glasses and Ferromagnets

A zero temperature dynamics of Ising spin glasses and ferromagnets on random graphs of finite connectivity is considered, like granular media these systems have an extensive entropy of metastable states. We consider the problem of what energy a randomly prepared spin system falls to before becoming stuck in a metastable state. We then introduce a tapping mechanism, analogous to that of real experiments on granular media, this tapping, corresponding to flipping simultaneously any spin with probability $p$, leads to stationary regime with a steady state energy $E(p)$. We explicitly solve this problem for the one dimensional ferromagnet and $\pm J$ spin glass and carry out extensive numerical simulations for spin systems of higher connectivity. The link with the density of metastable states at fixed energy and the idea of Edwards that one may construct a thermodynamics with a flat measure over metastable states is discussed. In addition our simulations on the ferromagnetic systems reveal a novel first order transition, whereas the usual thermodynamic transition on these graphs is second order.Comment: 11 pages, 7 figure

Scaling of the distribution of fluctuations of financial market indices

We study the distribution of fluctuations over a time scale $\Delta t$ (i.e., the returns) of the S&P 500 index by analyzing three distinct databases. Database (i) contains approximately 1 million records sampled at 1 min intervals for the 13-year period 1984-1996, database (ii) contains 8686 daily records for the 35-year period 1962-1996, and database (iii) contains 852 monthly records for the 71-year period 1926-1996. We compute the probability distributions of returns over a time scale $\Delta t$, where $\Delta t$ varies approximately over a factor of 10^4 - from 1 min up to more than 1 month. We find that the distributions for $\Delta t \leq$ 4 days (1560 mins) are consistent with a power-law asymptotic behavior, characterized by an exponent $\alpha \approx 3$, well outside the stable L\'evy regime $0 < \alpha < 2$. To test the robustness of the S&P result, we perform a parallel analysis on two other financial market indices. Database (iv) contains 3560 daily records of the NIKKEI index for the 14-year period 1984-97, and database (v) contains 4649 daily records of the Hang-Seng index for the 18-year period 1980-97. We find estimates of $\alpha$ consistent with those describing the distribution of S&P 500 daily-returns. One possible reason for the scaling of these distributions is the long persistence of the autocorrelation function of the volatility. For time scales longer than $(\Delta t)_{\times} \approx 4$ days, our results are consistent with slow convergence to Gaussian behavior.Comment: 12 pages in multicol LaTeX format with 27 postscript figures (Submitted to PRE May 20, 1999). See http://polymer.bu.edu/~amaral/Professional.html for more of our work on this are

Fatal COVID-19 outcomes are associated with an antibody response targeting epitopes shared with endemic coronaviruses

The role of immune responses to previously seen endemic coronavirus epitopes in severe acute respiratory coronavirus 2 (SARS-CoV-2) infection and disease progression has not yet been determined. Here, we show that a key characteristic of fatal coronavirus disease (COVID-19) outcomes is that the immune response to the SARS-CoV-2 spike protein is enriched for antibodies directed against epitopes shared with endemic beta-coronaviruses, and has a lower proportion of antibodies targeting the more protective variable regions of the spike. The magnitude of antibody responses to the SARS-CoV-2 full-length spike protein, its domains and subunits, and the SARS-CoV-2 nucleocapsid also correlated strongly with responses to the endemic beta-coronavirus spike proteins in individuals admitted to intensive care units (ICU) with fatal COVID-19 outcomes, but not in individuals with non-fatal outcomes. This correlation was found to be due to the antibody response directed at the S2 subunit of the SARS-CoV-2 spike protein, which has the highest degree of conservation between the beta-coronavirus spike proteins. Intriguingly, antibody responses to the less cross-reactive SARS-CoV-2 nucleocapsid were not significantly different in individuals who were admitted to ICU with fatal and non-fatal outcomes, suggesting an antibody profile in individuals with fatal outcomes consistent with an original antigenic sin type-response

Fatal COVID-19 outcomes are associated with an antibody response targeting epitopes shared with endemic coronaviruses.

The role of immune responses to previously seen endemic coronavirus epitopes in severe acute respiratory coronavirus 2 (SARS-CoV-2) infection and disease progression has not yet been determined. Here, we show that a key characteristic of fatal coronavirus disease (COVID-19) outcomes is that the immune response to the SARS-CoV-2 spike protein is enriched for antibodies directed against epitopes shared with endemic beta-coronaviruses, and has a lower proportion of antibodies targeting the more protective variable regions of the spike. The magnitude of antibody responses to the SARS-CoV-2 full-length spike protein, its domains and subunits, and the SARS-CoV-2 nucleocapsid also correlated strongly with responses to the endemic beta-coronavirus spike proteins in individuals admitted to intensive care units (ICU) with fatal COVID-19 outcomes, but not in individuals with non-fatal outcomes. This correlation was found to be due to the antibody response directed at the S2 subunit of the SARS-CoV-2 spike protein, which has the highest degree of conservation between the beta-coronavirus spike proteins. Intriguingly, antibody responses to the less cross-reactive SARS-CoV-2 nucleocapsid were not significantly different in individuals who were admitted to ICU with fatal and non-fatal outcomes, suggesting an antibody profile in individuals with fatal outcomes consistent with an original antigenic sin type-response

PDE2A2 regulates mitochondria morphology and apoptotic cell death via local modulation of cAMP/PKA signalling

cAMP/PKA signalling is compartmentalised with tight spatial and temporal control of signal propagation underpinning specificity of response. The cAMP-degrading enzymes, phosphodiesterases (PDEs), localise to specific subcellular domains within which they control local cAMP levels and are key regulators of signal compartmentalisation. Several components of the cAMP/PKA cascade are located to different mitochondrial sub-compartments, suggesting the presence of multiple cAMP/PKA signalling domains within the organelle. The function and regulation of these domains remain largely unknown. Here, we describe a novel cAMP/PKA signalling domain localised at mitochondrial membranes and regulated by PDE2A2. Using pharmacological and genetic approaches combined with real-time FRET imaging and high resolution microscopy we demonstrate that in rat cardiac myocytes and other cell types mitochondrial PDE2A2 regulates local cAMP levels and PKA-dependent phosphorylation of Drp1. We further demonstrate that inhibition of PDE2A, by enhancing the hormone-dependent cAMP response locally, affects mitochondria dynamics and protects from apoptotic cell death