7 research outputs found

    Western north pacific tropical cyclone tracks in cmip5 models : statistical assessment using a model-independent detection and tracking scheme

    Get PDF
    Past studies have shown that tropical cyclone (TC) projection results can be sensitive to different types of TC tracking schemes, and that the relative adjustments of detection criteria to accommodate different models may not necessarily provide a consistent platform for comparison of projection results. Here, future climate projections of TC activity in the western North Pacific basin (WNP, defined from 0°-50°NAND 100°E-180°) are assessed with a model-independent detection and tracking scheme. This scheme is applied to models from phase 5 of the Coupled Model Intercomparison Project (CMIP5) forced under the historical and representative concentration pathway 8.5 (RCP8.5) conditions. TC tracks from the observed records and independent models are analyzed simultaneously with a curve-clustering algorithm, allowing observed and model tracks to be projected onto the same set of clusters (k =9). Four of the nine clusters were projected to undergo significant changes in TC frequency. Straight-moving TCs in the South China Sea were projected to significantly decrease. Projected increases in TC frequency were found poleward of 20°N and east of 160°E, consistent with changes in ascending motion, as well as vertical wind shear and relative humidity respectively. Projections of TC track exposure indicated significant reductions for southern China and the Philippines and significant increases for the Korean peninsula and Japan, although very few model TCs reached the latter subtropical regions in comparison to the observations. The use of a fundamentally different detection methodology that overcomes the detector/tracker bias gives increased certainty to projections as best as lowresolution simulations can offer. © 2019 American Meteorological Society

    Participation as Post-Fordist Politics: Demos, New Labour, and Science Policy

    Get PDF
    In recent years, British science policy has seen a significant shift ‘from deficit to dialogue’ in conceptualizing the relationship between science and the public. Academics in the interdisciplinary field of Science and Technology Studies (STS) have been influential as advocates of the new public engagement agenda. However, this participatory agenda has deeper roots in the political ideology of the Third Way. A framing of participation as a politics suited to post-Fordist conditions was put forward in the magazine Marxism Today in the late 1980s, developed in the Demos thinktank in the 1990s, and influenced policy of the New Labour government. The encouragement of public participation and deliberation in relation to science and technology has been part of a broader implementation of participatory mechanisms under New Labour. This participatory program has been explicitly oriented toward producing forms of social consciousness and activity seen as essential to a viable knowledge economy and consumer society. STS arguments for public engagement in science have gained influence insofar as they have intersected with the Third Way politics of post-Fordism

    HIV-1–infected dendritic cells show 2 phases of gene expression changes, with lysosomal enzyme activity decreased during the second phase

    No full text
    Dendritic cells (DCs) play a key role in the pathogenesis of HIV infection. HIV interacts with these cells through 2 pathways in 2 temporal phases, initially via endocytosis and then via de novo replication. Here the transcriptional response of human DCs to HIV-1 was studied in these phases and at different stages of the virus replication cycle using purified HIV-1 envelope proteins, and inactivated and viable HIV-1. No differential gene expression was detected in response to envelope. However, more than 100 genes were differentially expressed in response to entry of viable and inactivated HIV-1 in the first phase. A completely different set of genes was differentially expressed in the second phase, predominantly in response to viable HIV-1, including up-regulation of immune regulation genes, whereas genes encoding lysosomal enzymes were down-regulated. Cathepsins B, C, S, and Z RNA and protein decreased, whereas cathepsin L was increased, probably reflecting a concomitant decrease in cystatin C. The net effect was markedly diminished cathepsin activity likely to result in enhanced HIV-1 survival and transfer to contacting T lymphocytes but decreased HIV-1 antigen processing and presentation to these T cells

    HIV-1 infection of human macrophages directly induces viperin which inhibits viral production

    No full text
    Macrophages are key target cells for HIV-1. HIV-1BaL induced a subset of interferon-stimulated genes in monocyte-derived macrophages (MDMs), which differed from that in monocyte-derived dendritic cells and CD4 T cells, without inducing any interferons. Inhibition of type I interferon induction was mediated by HIV-1 inhibition of interferon-regulated factor (IRF3) nuclear translocation. In MDMs, viperin was the most up-regulated interferon-stimulated genes, and it significantly inhibited HIV-1 production. HIV-1 infection disrupted lipid rafts via viperin induction and redistributed viperin to CD81 compartments, the site of HIV-1 egress by budding in MDMs. Exogenous farnesol, which enhances membrane protein prenylation, reversed viperin-mediated inhibition of HIV-1 production. Mutagenesis analysis in transfected cell lines showed that the internal S-adenosyl methionine domains of viperin were essential for its antiviral activity. Thus viperin may contribute to persistent noncytopathic HIV-1 infection of macrophages and possibly to biologic differences with HIV-1–infected T cells.Najla Nasr, Susan Maddocks, Stuart G. Turville, Andrew N. Harman, Natalie Woolger, Karla J.Helbig, John Wilkinson, Chris R. Bye, Thomas K. Wright, Dharshini Rambukwelle, Heather Donaghy, Michael R. Beard and Anthony L. Cunningha

    Tumor necrosis factor-alpha- and IL-4-independent development of Langerhans cell-like dendritic cells from M-CSF-conditioned precursors.

    Get PDF
    GM-CSF and transforming growth factor ÎČ (TGFÎČ) are required for the generation of Langerhans cells (LC), members of the dendritic cell (DC) family. Tumor necrosis factor α (TNFα) and IL-4 can enhance LC differentiation from human monocytes or CD34+ progenitors. Here, we show that M-CSF-cultured DC precursors derived from CD34+ progenitors resemble dermal CD14+ cells and readily convert to LC-like DC in GM-CSF/TGFÎČ. The cells express Langerin, CD1a, and CCR6, migrate in response to CCR6 ligand CCL20, and contain Birbeck granules. TNFα and IL-4, added separately or together, have an inhibitory effect on LC differentiation. Cells differentiated in the presence of IL-4 and TNFα express low levels of CCR7. This suggests that M-CSF-conditioned DC precursors retain the capacity to efficiently undergo a differentiation program, giving rise to LC-like DC solely through the effect of GM-CSF and TGFÎČ
    corecore