57 research outputs found

    Developing Scenarios for Product Longevity and Sufficiency

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    This paper explores the narrative of peoples’ relationships with products as a window on understanding the types of innovation that may inform a culture of sufficiency. The work forms part of the 'Business as Unusual: Designing Products with Consumers in the Loop' [BaU] project, funded as part of the UK EPSRC-ESRC RECODE network (RECODE, 2016) that aims to explore the potential of re-distributed manufacturing (RdM) in a context of sustainability. This element of the project employed interviews, mapping and workshops as methods to investigate the relationship between people and products across the product lifecycle. A focus on product longevity and specifically the people-product interactions is captured in conversations around product maintenance and repair. In exploring ideas of ‘broken’ we found different characteristics of, and motivations for, repair. Mapping these and other product-people interactions across the product lifecycle indicated where current activity is, who owns such activity (i.e. organisation or individual) and where gaps in interactions occur. These issues were explored further in a workshop which grouped participants to look at products from the perspective of one of four scenarios; each scenario represented either short or long product lifespans and different types of people engagement in the design process. The findings help give shape to new scenarios for designing sufficiency-based social models of material flows

    A landscape of repair

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    This paper reports on EPSRC-funded research that explores the role of repair in creating new models of sustainable business. In the lifecycle stage of repair we explore what 'broken' means and uncover the nature of local and dispersed repair activities. This in turn allows us to better understand how the relationship between products and people can help shape new modes of consumption. Therefore, narratives of repair are collected to identify diverse people-product interactions and illustrate the different characteristics of, and motivations for, repair. The paper proposes that mapping the different product-people interactions across the product lifecycle, particularly at the stage of fragile-functionality (performance or function failure, emotional disengagement, superseded technology) is important in understanding the potential for enduring products and their repair. Building a landscape of repair creates new opportunities for manufacture and for slowing resource loops across product lifetimes, which together provide a framework for a sufficiency-based model of production and consumption

    MASP-1 Induces a Unique Cytokine Pattern in Endothelial Cells: A Novel Link between Complement System and Neutrophil Granulocytes

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    Microbial infection urges prompt intervention by the immune system. The complement cascade and neutrophil granulocytes are the predominant contributors to this immediate anti-microbial action. We have previously shown that mannan-binding lectin-associated serine protease-1 (MASP-1), the most abundant enzyme of the complement lectin pathway, can induce p38-MAPK activation, NFkappaB signaling, and Ca(2+)-mobilization in endothelial cells. Since neutrophil chemotaxis and transmigration depends on endothelial cell activation, we aimed to explore whether recombinant MASP-1 (rMASP-1) is able to induce cytokine production and subsequent neutrophil chemotaxis in human umbilical vein endothelial cells (HUVEC). We found that HUVECs activated by rMASP-1 secreted IL-6 and IL-8, but not IL-1alpha, IL-1ra, TNFalpha and MCP-1. rMASP-1 induced dose-dependent IL-6 and IL-8 production with different kinetics. rMASP-1 triggered IL-6 and IL-8 production was regulated predominantly by the p38-MAPK pathway. Moreover, the supernatant of rMASP-1-stimulated HUVECs activated the chemotaxis of neutrophil granulocytes as an integrated effect of cytokine production. Our results implicate that besides initializing the complement lectin pathway, MASP-1 may activate neutrophils indirectly, via the endothelial cells, which link these effective antimicrobial host defense mechanisms

    Genetic polymorphisms of the RAS-cytokine pathway and chronic kidney disease

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    Chronic kidney disease (CKD) in children is irreversible. It is associated with renal failure progression and atherosclerotic cardiovascular (CV) abnormalities. Nearly 60% of children with CKD are affected since birth with congenital or inherited kidney disorders. Preliminary evidence primarily from adult CKD studies indicates common genetic risk factors for CKD and atherosclerotic CV disease. Although multiple physiologic pathways share common genes for CKD and CV disease, substantial evidence supports our attention to the renin angiotensin system (RAS) and the interlinked inflammatory cascade because they modulate the progressions of renal and CV disease. Gene polymorphisms in the RAS-cytokine pathway, through altered gene expression of inflammatory cytokines, are potential factors that modulate the rate of CKD progression and CV abnormalities in patients with CKD. For studying such hypotheses, the cooperative efforts among scientific groups and the availability of robust and affordable technologies to genotype thousands of single nucleotide polymorphisms (SNPs) across the genome make genome-wide association studies an attractive paradigm for studying polygenic diseases such as CKD. Although attractive, such studies should be interpreted carefully, with a fundamental understanding of their potential weaknesses. Nevertheless, whole-genome association studies for diabetic nephropathy and future studies pertaining to other types of CKD will offer further insight for the development of targeted interventions to treat CKD and associated atherosclerotic CV abnormalities in the pediatric CKD population

    Genetic variation and exercise-induced muscle damage: implications for athletic performance, injury and ageing.

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    Prolonged unaccustomed exercise involving muscle lengthening (eccentric) actions can result in ultrastructural muscle disruption, impaired excitation-contraction coupling, inflammation and muscle protein degradation. This process is associated with delayed onset muscle soreness and is referred to as exercise-induced muscle damage. Although a certain amount of muscle damage may be necessary for adaptation to occur, excessive damage or inadequate recovery from exercise-induced muscle damage can increase injury risk, particularly in older individuals, who experience more damage and require longer to recover from muscle damaging exercise than younger adults. Furthermore, it is apparent that inter-individual variation exists in the response to exercise-induced muscle damage, and there is evidence that genetic variability may play a key role. Although this area of research is in its infancy, certain gene variations, or polymorphisms have been associated with exercise-induced muscle damage (i.e. individuals with certain genotypes experience greater muscle damage, and require longer recovery, following strenuous exercise). These polymorphisms include ACTN3 (R577X, rs1815739), TNF (-308 G>A, rs1800629), IL6 (-174 G>C, rs1800795), and IGF2 (ApaI, 17200 G>A, rs680). Knowing how someone is likely to respond to a particular type of exercise could help coaches/practitioners individualise the exercise training of their athletes/patients, thus maximising recovery and adaptation, while reducing overload-associated injury risk. The purpose of this review is to provide a critical analysis of the literature concerning gene polymorphisms associated with exercise-induced muscle damage, both in young and older individuals, and to highlight the potential mechanisms underpinning these associations, thus providing a better understanding of exercise-induced muscle damage
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