Intrusion triggering of the 2010 Eyjafjallajökull explosive eruption

Gradual inflation of magma chambers often precedes eruptions at highly active volcanoes. During such eruptions, rapid deflation occurs as magma flows out and pressure is reduced. Less is known about the deformation style at moderately active volcanoes, such as Eyjafjallaj?kull, Iceland, where an explosive summit eruption of trachyandesite beginning on 14 April 2010 caused exceptional disruption to air traffic, closing airspace over much of Europe for days. This eruption was preceded by an effusive flank eruption of basalt from 20 March to 12 April 2010. The 2010 eruptions are the culmination of 18?years of intermittent volcanic unrest. Here we show that deformation associated with the eruptions was unusual because it did not relate to pressure changes within a single magma chamber. Deformation was rapid before the first eruption (>5?mm per day after 4 March), but negligible during it. Lack of distinct co-eruptive deflation indicates that the net volume of magma drained from shallow depth during this eruption was small; rather, magma flowed from considerable depth. Before the eruption, a ～0.05?km(3) magmatic intrusion grew over a period of three months, in a temporally and spatially complex manner, as revealed by GPS (Global Positioning System) geodetic measurements and interferometric analysis of satellite radar images. The second eruption occurred within the ice-capped caldera of the volcano, with explosivity amplified by magma-ice interaction. Gradual contraction of a source, distinct from the pre-eruptive inflation sources, is evident from geodetic data. Eyjafjallaj?kull's behaviour can be attributed to its off-rift setting with a 'cold' subsurface structure and limited magma at shallow depth, as may be typical for moderately active volcanoes. Clear signs of volcanic unrest signals over years to weeks may indicate reawakening of such volcanoes, whereas immediate short-term eruption precursors may be subtle and difficult to detect.     

Transiting circumbinary planets Kepler-34 b and Kepler-35 b

Most Sun-like stars in the Galaxy reside in gravitationally bound pairs of stars (binaries). Although long anticipated, the existence of a 'circumbinary planet' orbiting such a pair of normal stars was not definitively established until the discovery of the planet transiting (that is, passing in front of) Kepler-16. Questions remained, however, about the prevalence of circumbinary planets and their range of orbital and physical properties. Here we report two additional transiting circumbinary planets: Kepler-34 (AB)b and Kepler-35 (AB)b, referred to here as Kepler-34 b and Kepler-35 b, respectively. Each is a low-density gas-giant planet on an orbit closely aligned with that of its parent stars. Kepler-34 b orbits two Sun-like stars every 289?days, whereas Kepler-35 b orbits a pair of smaller stars (89% and 81% of the Sun's mass) every 131?days. The planets experience large multi-periodic variations in incident stellar radiation arising from the orbital motion of the stars. The observed rate of circumbinary planets in our sample implies that more than ～1% of close binary stars have giant planets in nearly coplanar orbits, yielding a Galactic population of at least several million.     

Supercurrent reversal in quantum dots

When two superconductors are electrically connected by a weak link--such as a tunnel barrier--a zero-resistance supercurrent can flow. This supercurrent is carried by Cooper pairs of electrons with a combined charge of twice the elementary charge, e. The 2e charge quantum is clearly visible in the height of voltage steps in Josephson junctions under microwave irradiation, and in the magnetic flux periodicity of h/2e (where h is Planck's constant) in superconducting quantum interference devices. Here we study supercurrents through a quantum dot created in a semiconductor nanowire by local electrostatic gating. Owing to strong Coulomb interaction, electrons only tunnel one-by-one through the discrete energy levels of the quantum dot. This nevertheless can yield a supercurrent when subsequent tunnel events are coherent. These quantum coherent tunnelling processes can result in either a positive or a negative supercurrent, that is, in a normal or a pi-junction, respectively. We demonstrate that the supercurrent reverses sign by adding a single electron spin to the quantum dot. When excited states of the quantum dot are involved in transport, the supercurrent sign also depends on the character of the orbital wavefunctions.     

Review： Protein folding pathology in domestic animals

Fibrillar proteins form structural elements of cells and the extracellular matrix. Pathological lesions of fibrillar microanatomical structures, or secondary fibrillar changes in globular proteins are well known. A special group concerns histologically amorphous deposits, amyloid. The major characteristics of amyloid are: apple green birefringence after Congo red staining of histological sections, and non-branching 7-10nm thick fibrils on electron microscopy revealing a high content of cross beta pleated sheets. About 25 different types of amyloid have been characterised. In animals, AA-amyloid is the most frequent type. Other types of amyloid in animals represent: AIAPP (in cats), AApoAⅠ, AApoAⅡ, localised AL-amyloid, amyloid in odontogenic or mammary tumors and amyloid in the brain. In old dogs Aβ and in sheep APrP^sc-amyloid can be encountered. AA-amyloidosis is a systemic disorder with a precursor in blood, acute phase serum amyloid A (SAA). In chronic inflammatory processes AA-amyloid can be deposited. A rapid crystallization of SAA to amyloid fibrils on small beta-sheeted fragments, the ‘amyloid enhancing factor‘ (AEF), is known and the AEF has been shown to penetrate the enteric barrier. Amyloid fibrils can aggregate from various precursor proteins in vitro in particular at acidic pH and when proteolytic fragments are formed. Molecular chaperones influence this process. Tissue data point to amyloid fibrillogenesis in lysosomes and near cell surfaces. A comparison can be made of the fibrillogenesis in prion diseases and in enhanced AA-amyloidosis. In the reactive form, acute phase SAA is the supply of the precursor protein, whereas in the prion diseases, cell membrane proteins form a structural source. AI3-amyloid in brain tissue of aged dogs showing signs of dementia forms a canine counterpart of senile dementia of the Alzheimer type (ccSDAT) in man. Misfolded proteins remain potential food hazards. Developments concerning prevention of amyloidogenesis and therapy of amyloid deposits are shortly commented.     

Vapour undersaturation in primitive mid-ocean-ridge basalt and the volatile content of Earth's upper mantle

The analysis of volatiles in magmatic systems can be used to constrain the volatile content of the Earth's mantle and the influence that magmatic degassing has on the chemistry of the oceans and the atmosphere. But most volatile elements have very low solubilities in magmas at atmospheric pressure, and therefore virtually all erupted lavas are degassed and do not retain their primary volatile signatures. Here we report the undersaturated pre-eruptive volatile content for a suite of mid-ocean-ridge basalts from the Siqueiros intra-transform spreading centre. The undersaturation leads to correlations between volatiles and refractory trace elements that provide new constraints on volatile abundances and their behaviour in the upper mantle. Our data generate improved limits on the abundances of carbon dioxide, water, fluorine, sulphur and chlorine in the source of normal mid-ocean-ridge basalt. The incompatible behaviour of carbon dioxide, together with the CO(2)/Nb and CO(2)/Cl ratios, permit estimates of primitive carbon dioxide and chlorine to be made for degassed and chlorine-contaminated mid-ocean-ridge basalt magmas, and hence constrain degassing and contamination histories of mid-ocean ridges.     

引力向量与引力张量的三维笛卡儿坐标表示式

导出了引力向量和引力张量球谐函数展开式的三维笛卡儿坐标表示公式 ,并给出了该表示式在两极和赤道的简化形式 .引力向量和引力张量的三维笛卡儿坐标表示式在形式上比球坐标表示式简单 ,且便于表示卫星的三维笛卡儿坐标系摄动量与位系数的关系     

Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death

Huntington's disease is caused by an abnormal polyglutamine expansion within the protein huntingtin and is characterized by microscopic inclusion bodies of aggregated huntingtin and by the death of selected types of neuron. Whether inclusion bodies are pathogenic, incidental or a beneficial coping response is controversial. To resolve this issue we have developed an automated microscope that returns to precisely the same neuron after arbitrary intervals, even after cells have been removed from the microscope stage. Here we show, by survival analysis, that neurons die in a time-independent fashion but one that is dependent on mutant huntingtin dose and polyglutamine expansion; many neurons die without forming an inclusion body. Rather, the amount of diffuse intracellular huntingtin predicts whether and when inclusion body formation or death will occur. Surprisingly, inclusion body formation predicts improved survival and leads to decreased levels of mutant huntingtin elsewhere in a neuron. Thus, inclusion body formation can function as a coping response to toxic mutant huntingtin.     

Herpesvirus latency confers symbiotic protection from bacterial infection

All humans become infected with multiple herpesviruses during childhood. After clearance of acute infection, herpesviruses enter a dormant state known as latency. Latency persists for the life of the host and is presumed to be parasitic, as it leaves the individual at risk for subsequent viral reactivation and disease. Here we show that herpesvirus latency also confers a surprising benefit to the host. Mice latently infected with either murine gammaherpesvirus 68 or murine cytomegalovirus, which are genetically highly similar to the human pathogens Epstein-Barr virus and human cytomegalovirus, respectively, are resistant to infection with the bacterial pathogens Listeria monocytogenes and Yersinia pestis. Latency-induced protection is not antigen specific but involves prolonged production of the antiviral cytokine interferon-gamma and systemic activation of macrophages. Latency thereby upregulates the basal activation state of innate immunity against subsequent infections. We speculate that herpesvirus latency may also sculpt the immune response to self and environmental antigens through establishment of a polarized cytokine environment. Thus, whereas the immune evasion capabilities and lifelong persistence of herpesviruses are commonly viewed as solely pathogenic, our data suggest that latency is a symbiotic relationship with immune benefits for the host.