63 research outputs found

    Thermodynamic Limits on Magnetodynamos in Rocky Exoplanets

    Full text link
    To ascertain whether magnetic dynamos operate in rocky exoplanets more massive or hotter than the Earth, we developed a parametric model of a differentiated rocky planet and its thermal evolution. Our model reproduces the established properties of Earth's interior and magnetic field at the present time. When applied to Venus, assuming that planet lacks plate tectonics and has a dehydrated mantle with an elevated viscosity, the model shows that the dynamo shuts down or never operated. Our model predicts that at a fixed planet mass, dynamo history is sensitive to core size, but not to the initial inventory of long-lived, heat-producing radionuclides. It predicts that rocky planets larger than 2.5 Earth masses will not develop inner cores because the temperature-pressure slope of the iron solidus becomes flatter than that of the core adiabat. Instead, iron "snow" will condense near or at the top of these cores, and the net transfer of latent heat upwards will suppress convection and a dynamo. More massive planets can have anemic dynamos due to core cooling, but only if they have mobile lids (plate tectonics). The lifetime of these dynamos is shorter with increasing planet mass but longer with higher surface temperature. Massive Venus-like planets with stagnant lids and more viscous mantles will lack dynamos altogether. We identify two alternative sources of magnetic fields on rocky planets: eddy currents induced in the hot or molten upper layers of planets on very short period orbits, and dynamos in the ionic conducting layers of "ocean" planets with ~10% mass in an upper mantle of water (ice).Comment: Accepted to The Astrophysical Journa

    Influenza A Virus Lacking the NS1 Gene Replicates in Interferon-Deficient Systems

    Get PDF
    AbstractThe NS1 protein is the only nonstructural protein encoded by influenza A virus. It has been proposed that the NS1 performs several regulatory functions during the viral replication cycle, including the regulation of synthesis, transport, splicing, and translation of mRNAs. Through the use of reverse genetics, a viable transfectant influenza A virus (delNS1) which lacks the NS1 gene has been generated. Our results indicate that the NS1 of influenza A virus is an auxiliary (virulence) factor which plays a crucial role in inhibiting interferon-mediated antiviral responses of the host

    Thermal and electrical conductivity of solid iron and iron-silicon mixtures at Earth's core conditions

    Get PDF
    We report on the thermal and electrical conductivities of solid iron and iron–silicon mixtures (Fe0.92Si0.08 and Fe0.93Si0.07), representative of the composition of the Earth's solid inner core at the relevant pressure–temperature conditions, obtained from density functional theory calculations with the Kubo–Greenwood formulation. We find thermal conductivities View the MathML source, and electrical conductivities View the MathML source at the top of the inner core (centre of the Earth). These values are respectively about 45–56% and 18–25% higher than the corresponding conductivities in the liquid outer core. The higher conductivities are due to the solid structure and to the lower concentration of light impurities. These values are much higher than those in use for previous inner core studies, k by a factor of four and σ by a factor of three. The high thermal conductivity means that heat leaks out by conduction almost as quickly as the inner core forms, making thermal convection unlikely. The high electrical conductivity increases the magnetic decay time of the inner core by a factor of more than three, lengthening the magnetic diffusion time to 10 kyr and making it more likely that the inner core stabilises the geodynamo and reduces the frequency of reversals

    Intranasal Delivery of Influenza Subunit Vaccine Formulated with GEM Particles as an Adjuvant

    Get PDF
    Nasal administration of influenza vaccine has the potential to facilitate influenza control and prevention. However, when administered intranasally (i.n.), commercially available inactivated vaccines only generate systemic and mucosal immune responses if strong adjuvants are used, which are often associated with safety problems. We describe the successful use of a safe adjuvant Gram-positive enhancer matrix (GEM) particles derived from the food-grade bacterium Lactococcus lactis for i.n. vaccination with subunit influenza vaccine in mice. It is shown that simple admixing of the vaccine with the GEM particles results in a strongly enhanced immune response. Already after one booster, the i.n. delivered GEM subunit vaccine resulted in hemagglutination inhibition titers in serum at a level equal to the conventional intramuscular (i.m.) route. Moreover, i.n. immunization with GEM subunit vaccine elicited superior mucosal and Th1 skewed immune responses compared to those induced by i.m. and i.n. administered subunit vaccine alone. In conclusion, GEM particles act as a potent adjuvant for i.n. influenza immunization

    Lack of Bax Prevents Influenza A Virus-Induced Apoptosis and Causes Diminished Viral Replication ▿

    No full text
    The ectopic overexpression of Bcl-2 restricts both influenza A virus-induced apoptosis and influenza A virus replication in MDCK cells, thus suggesting a role for Bcl-2 family members during infection. Here we report that influenza A virus cannot establish an apoptotic response without functional Bax, a downstream target of Bcl-2, and that both Bax and Bak are directly involved in influenza A virus replication and virus-induced cell death. Bak is substantially downregulated during influenza A virus infection in MDCK cells, and the knockout of Bak in mouse embryonic fibroblasts yields a dramatic rise in the rate of apoptotic death and a corresponding increase in levels of virus replication, suggesting that Bak suppresses both apoptosis and the replication of virus and that the virus suppresses Bak. Bax, however, is activated and translocates from the cytosol to the mitochondria; this activation is required for the efficient induction of apoptosis and virus replication. The knockout of Bax in mouse embryonic fibroblasts blocks the induction of apoptosis, restricts the infection-mediated activation of executioner caspases, and inhibits virus propagation. Bax knockout cells still die but by an alternative death pathway displaying characteristics of autophagy, similarly to our previous observation that influenza A virus infection in the presence of a pancaspase inhibitor leads to an increase in levels of autophagy. The knockout of Bax causes a retention of influenza A virus NP within the nucleus. We conclude that the cell and virus struggle to control apoptosis and autophagy, as appropriately timed apoptosis is important for the replication of influenza A virus
    corecore