868 research outputs found

    Meeting the costs of decarbonising industry – The potential effects on prices and competitiveness (a case study of the UK)

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    Industry produces a third of global greenhouse gas emissions and needs to be decarbonised as countries strive for net zero. But how might the costs of this be met and what effect might the options have on businesses and consumers? Using the UK as a case study, we investigate the relative effect on prices and profit margins of three idealised illustrative scenarios for distributing the costs of decarbonising industry: (1) absorbing them, (2) passing them on to consumers, and (3) sharing them along the relevant value chains. To do this, we combine direct process cost projections from a detailed industry pathway model (covering 115 sector-process combinations and 96 unique low-carbon technologies) with techniques exploiting multi-regional input-output analysis. Industrial decarbonisation consistent with net-zero goals can be achieved with an aggregate increase in prices as low as 0.8%, and minimal impact on equality. However, the impact on some industries is more pronounced; while costs might be beneficially shared between sectors to some extent, some will find this more challenging. The findings are relevant to industrial decarbonisation policies and the support they need to provide, the effects that industrial decarbonisation might have on equality, and its potential effect on international competition

    PARP1 gene variation and microglial activity on [11C]PBR28 PET in older adults at risk for Alzheimer's disease

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    Increasing evidence suggests that inflammation is one pathophysio-logical mechanism in Alzheimer's disease (AD). Recent studies have identified an association between the poly (ADP-ribose) polymerase 1 (PARP1) gene and AD. This gene encodes a protein that is involved in many biological functions, including DNA repair and chromatin remodeling, and is a mediator of inflammation. Therefore, we performed a targeted genetic association analysis to investigate the relationship between the PARP1 polymorphisms and brain micro-glial activity as indexed by [11C]PBR28 positron emission tomography (PET). Participants were 26 non-Hispanic Caucasians in the Indiana Memory and Aging Study (IMAS). PET data were intensity-normalized by injected dose/total body weight. Average PBR standardized uptake values (SUV) from 6 bilateral regions of interest (thalamus, frontal, parietal, temporal, and cingulate cortices, and whole brain gray matter) were used as endophenotypes. Single nucleotide polymorphisms (SNPs) with 20% minor allele frequency that were within +/− 20 kb of the PARP1 gene were included in the analyses. Gene-level association analyses were performed using a dominant genetic model with translocator protein (18-kDa) (TSPO) genotype, age at PET scan, and gender as covariates. Analyses were performed with and without APOE Δ4 status as a covariate. Associations with PBR SUVs from thalamus and cingulate were significant at corrected p<0.014 and <0.065, respectively. Subsequent multi-marker analysis with cingulate PBR SUV showed that individuals with the “C” allele at rs6677172 and “A” allele at rs61835377 had higher PBR SUV than individuals without these alleles (corrected P<0.03), and individuals with the “G” allele at rs6677172 and “G” allele at rs61835377 displayed the opposite trend (corrected P<0.065). A previous study with the same cohort showed an inverse relationship between PBR SUV and brain atrophy at a follow-up visit, suggesting possible protective effect of microglial activity against cortical atrophy. Interestingly, all 6 AD and 2 of 3 LMCI participants in the current analysis had one or more copies of the “GG” allele combination, associated with lower cingulate PBR SUV, suggesting that this gene variant warrants further investigation

    The rotational modes of relativistic stars: Numerical results

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    We study the inertial modes of slowly rotating, fully relativistic compact stars. The equations that govern perturbations of both barotropic and non-barotropic models are discussed, but we present numerical results only for the barotropic case. For barotropic stars all inertial modes are a hybrid mixture of axial and polar perturbations. We use a spectral method to solve for such modes of various polytropic models. Our main attention is on modes that can be driven unstable by the emission of gravitational waves. Hence, we calculate the gravitational-wave growth timescale for these unstable modes and compare the results to previous estimates obtained in Newtonian gravity (i.e. using post-Newtonian radiation formulas). We find that the inertial modes are slightly stabilized by relativistic effects, but that previous conclusions concerning eg. the unstable r-modes remain essentially unaltered when the problem is studied in full general relativity.Comment: RevTeX, 29 pages, 31 eps figure

    The Self Model and the Conception of Biological Identity in Immunology

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    The self/non-self model, first proposed by F.M. Burnet, has dominated immunology for sixty years now. According to this model, any foreign element will trigger an immune reaction in an organism, whereas endogenous elements will not, in normal circumstances, induce an immune reaction. In this paper we show that the self/non-self model is no longer an appropriate explanation of experimental data in immunology, and that this inadequacy may be rooted in an excessively strong metaphysical conception of biological identity. We suggest that another hypothesis, one based on the notion of continuity, gives a better account of immune phenomena. Finally, we underscore the mapping between this metaphysical deflation from self to continuity in immunology and the philosophical debate between substantialism and empiricism about identity

    Co-inhibition of TGF-ÎČ and PD-L1 pathways in a metastatic colorectal cancer mouse model triggers interferon responses, innate cells and T cells, alongside metabolic changes and tumor resistance

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    Colorectal cancer (CRC) is the third most prevalent cancer worldwide with a high mortality rate (20–30%), especially due to metastasis to adjacent organs. Clinical responses to chemotherapy, radiation, targeted and immunotherapies are limited to a subset of patients making metastatic CRC (mCRC) difficult to treat. To understand the therapeutic modulation of immune response in mCRC, we have used a genetically engineered mouse model (GEMM), “KPN”, which resembles the human ‘CMS4’-like subtype. We show here that transforming growth factor (TGF-ÎČ1), secreted by KPN organoids, increases cancer cell proliferation, and inhibits splenocyte activation in vitro. TGF-ÎČ1 also inhibits activation of naive but not pre-activated T cells, suggesting differential effects on specific immune cells. In vivo, the inhibition of TGF-ÎČ inflames the KPN tumors, causing infiltration of T cells, monocytes and monocytic intermediates, while reducing neutrophils and epithelial cells. Co-inhibition of TGF-ÎČ and PD-L1 signaling further enhances cytotoxic CD8+T cells and upregulates innate immune response and interferon gene signatures. However, simultaneous upregulation of cancer-related metabolic genes correlated with limited control of tumor burden and/or progression despite combination treatment. Our study illustrates the importance of using GEMMs to predict better immunotherapies for mCRC

    Responsible research and innovation in the digital age

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    At a time when increasingly potent technologies are being developed with the potential to transform society, researchers in all technological fields, including information and communications technology (ICT), are under growing pressure to consider and reflect on the motivations, purposes, and possible consequences associated with their research. This pressure comes from the general public, civil society, and government institutions. In parallel is a growing recognition that current ethics review procedures within ICT may not address broader concerns (such as the potential societal consequences of innovation)
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