84,002 research outputs found

    Space weather challenges of the polar cap ionosphere

    Get PDF
    This paper presents research on polar cap ionosphere space weather phenomena conducted during the European Cooperation in Science and Technology (COST) action ES0803 from 2008 to 2012. The main part of the work has been directed toward the study of plasma instabilities and scintillations in association with cusp flow channels and polar cap electron density structures/patches,which is considered as critical knowledge in order to develop forecast models for scintillations in the polar cap. We have approached this problem by multi-instrument techniques that comprise the EISCAT Svalbard Radar, SuperDARN radars, in-situ rocket, and GPS scintillation measurements. The Discussion section aims to unify the bits and pieces of highly specialized information from several papers into a generalized picture. The cusp ionosphere appears as a hot region in GPS scintillation climatology maps. Our results are consistent with the existing view that scintillations in the cusp and the polar cap ionosphere are mainly due to multi-scale structures generated by instability processes associated with the cross-polar transport of polar cap patches. We have demonstrated that the SuperDARN convection model can be used to track these patches backward and forward in time. Hence, once a patch has been detected in the cusp inflow region, SuperDARN can be used to forecast its destination in the future. However, the high-density gradient of polar cap patches is not the only prerequisite for high-latitude scintillations. Unprecedented high resolution rocket measurements reveal that the cusp ionosphere is associated with filamentary precipitation giving rise to kilometer scale gradients onto which the gradient drift instability can operate very efficiently... (continued

    A nongenomic mechanism for progesterone-mediated immunosuppression: Inhibition of K+ channels, Ca2+ signaling, and gene expression in T lymphocytes

    Get PDF
    The mechanism by which progesterone causes localized suppression of the immune response during pregnancy has remained elusive. Using human T lymphocytes and T cell lines, we show that progesterone, at concentrations found in the placenta, rapidly and reversibly blocks voltage-gated and calcium-activated K+ channels (KV and KCa, respectively), resulting in depolarization of the membrane potential. As a result, Ca2+ signaling and nuclear factor of activated T cells (NF-AT)-driven gene expression are inhibited. Progesterone acts distally to the initial steps of T cell receptor (TCR)-mediated signal transduction, since it blocks sustained Ca2+ signals after thapsigargin stimulation, as well as oscillatory Ca2+ signals, but not the Ca2+ transient after TCR stimulation. K+ channel blockade by progesterone is specific; other steroid hormones had little or no effect, although the progesterone antagonist RU 486 also blocked KV and KCa channels. Progesterone effectively blocked a broad spectrum of K+ channels, reducing both Kv1.3 and charybdotoxin-resistant components of KV current and KCa current in T cells, as well as blocking several cloned KV channels expressed in cell lines. Progesterone had little or no effect on a cloned voltage-gated Na+ channel, an inward rectifier K+ channel, or on lymphocyte Ca2+ and Cl- channels. We propose that direct inhibition of K+ channels in T cells by progesterone contributes to progesterone-induced immunosuppression

    Upregulation of Functional Kv11.1 Isoform Expression by Inhibition of Intronic Polyadenylation with Antisense Morpholino Oligonucleotides

    Full text link
    The KCNH2 gene encodes the Kv11.1 potassium channel that conducts the rapidly activating delayed rectifier current in the heart. KCNH2 pre-mRNA undergoes alternative processing; intron 9 splicing leads to the formation of a functional, full-length Kv11.1a isoform, while polyadenylationwithin intron 9 generates a non-functional, Cterminally truncated Kv11.1a-USO isoform. The relative expression of Kv11.1 isoforms plays an important role in the regulation of Kv11.1 channel function and the pathogenesis of long QT syndrome. In this study,we identified cis-acting elements that are required for KCNH2 intron 9 poly(A) signal activity. Mutation of these elements decreased Kv11.1a-USO expression and increased the expression of Kv11.1a mRNA, protein and channel current. More importantly, blocking these elements by antisense morpholino oligonucleotides shifted the alternative processing of KCNH2 intron 9 from the polyadenylation to the splicing pathway, leading to the predominant production of Kv11.1a and a significant increase in Kv11.1 current. Our findings indicate that the expression of the Kv11.1a isoform can be upregulated by an antisense approach. Antisense inhibition of KCNH2 intronic polyadenylation represents a novel approach to increase Kv11.1 channel function

    Dark matter from gravitational particle production at reheating

    Full text link
    We show that curvature induced particle production at reheating generates adiabatic dark matter if there are non-minimally coupled spectator scalars weakly coupled to visible matter. The observed dark matter abundance implies an upper bound on spectator masses mm and non-minimal coupling values ξ\xi. For example, assuming quadratic inflation, instant reheating and a single spectator scalar with only gravitational couplings, the observed dark matter abundance is obtained for m0.1m\sim 0.1 GeV and ξ1\xi \sim 1. Larger mass and coupling values of the spectator are excluded as they would lead to overproduction of dark matter.Comment: 10 pages, 1 figure. v2: updated references. v3: substantial modifications, results and conclusions partially changed but bounds on spectator fields almost unaffected. New title. v4: expanded discussion, accepted for publication in JCA

    Alaska after Prudhoe Bay: Sustainability of an Island Economy

    Get PDF
    A paper presented at the Annual Meeting of the Western Regional Science Association Monterey, CaliforniaThe typical sovereign island economy is small and remote. For example the remote island nations of Nauru, Niue, and Saint Helena have populations in the range of 10 thousand each. Of course not all island nations are small or remote and neither are small or remote economies necessarily islands. However it is useful to think about the economies of small and remote islands because they can help us to understand the economic structure and prospects of larger and less remote places. Island economies generally lack a comparative advantage in the production of goods or services for export to the rest of the world. This is due to distance from markets and suppliers as well as an absence of economies of scale and specialization, both of which drive up the cost of exporting goods and services. And although the economic theory of comparative advantage tells us that trade among countries can occur even if one has an advantage in the production of all goods and services, that theory can break down if costs in the small and remote economy are too high. The mechanism by which the island economy gains access to export markets in the presence of high costs is through downward adjustment in the wage. But in some cases the wage would need to become negative to overcome the cost disadvantages created by distance and size. In such a case the island would have a subsistence economy with neither exports to the rest of the world or imports. The most important private economic activities one observes in these economies are agriculture and fishing. Occasionally an island economy will be able to take advantage of a market niche to generate exports. Tourism is the most common, and mining has provided an export base in some other places. However these market activities will not necessarily be large enough to employ a large share of the population. Furthermore dependence on a single activity leaves these economies vulnerable or “precarious”.As a consequence many of these economies are dependent on foreign aid and remittances from emigrants. These funds allow these economies to purchase a basic level of imports that would not otherwise be possibleNorthrim Bank. University of Alaska Foundation

    Capacitance fluctuations causing channel noise reduction in stochastic Hodgkin-Huxley systems

    Full text link
    Voltage-dependent ion channels determine the electric properties of axonal cell membranes. They not only allow the passage of ions through the cell membrane but also contribute to an additional charging of the cell membrane resulting in the so-called capacitance loading. The switching of the channel gates between an open and a closed configuration is intrinsically related to the movement of gating charge within the cell membrane. At the beginning of an action potential the transient gating current is opposite to the direction of the current of sodium ions through the membrane. Therefore, the excitability is expected to become reduced due to the influence of a gating current. Our stochastic Hodgkin-Huxley like modeling takes into account both the channel noise -- i.e. the fluctuations of the number of open ion channels -- and the capacitance fluctuations that result from the dynamics of the gating charge. We investigate the spiking dynamics of membrane patches of variable size and analyze the statistics of the spontaneous spiking. As a main result, we find that the gating currents yield a drastic reduction of the spontaneous spiking rate for sufficiently large ion channel clusters. Consequently, this demonstrates a prominent mechanism for channel noise reduction.Comment: 18 page
    corecore