Little or no solar wind enters Venus' atmosphere at solar minimum

Venus has no significant internal magnetic field, which allows the solar wind to interact directly with its atmosphere. A field is induced in this interaction, which partially shields the atmosphere, but we have no knowledge of how effective that shield is at solar minimum. (Our current knowledge of the solar wind interaction with Venus is derived from measurements at solar maximum.) The bow shock is close to the planet, meaning that it is possible that some solar wind could be absorbed by the atmosphere and contribute to the evolution of the atmosphere. Here we report magnetic field measurements from the Venus Express spacecraft in the plasma environment surrounding Venus. The bow shock under low solar activity conditions seems to be in the position that would be expected from a complete deflection by a magnetized ionosphere. Therefore little solar wind enters the Venus ionosphere even at solar minimum.     

Snapshots of nuclear pore complexes in action captured by cryo-electron tomography

Nuclear pore complexes reside in the nuclear envelope of eukaryotic cells and mediate the nucleocytoplasmic exchange of macromolecules. Traffic is regulated by mobile transport receptors that target their cargo to the central translocation channel, where phenylalanine-glycine-rich repeats serve as binding sites. The structural analysis of the nuclear pore is a formidable challenge given its size, its location in a membranous environment and its dynamic nature. Here we have used cryo-electron tomography to study the structure of nuclear pore complexes in their functional environment, that is, in intact nuclei of Dictyostelium discoideum. A new image-processing strategy compensating for deviations of the asymmetric units (protomers) from a perfect eight-fold symmetry enabled us to refine the structure and to identify new features. Furthermore, the superposition of a large number of tomograms taken in the presence of cargo, which was rendered visible by gold nanoparticles, has yielded a map outlining the trajectories of import cargo. Finally, we have performed single-molecule Monte Carlo simulations of nuclear import to interpret the experimentally observed cargo distribution in the light of existing models for nuclear import.     

Dll4 signalling through Notch1 regulates formation of tip cells during angiogenesis

In sprouting angiogenesis, specialized endothelial tip cells lead the outgrowth of blood-vessel sprouts towards gradients of vascular endothelial growth factor (VEGF)-A. VEGF-A is also essential for the induction of endothelial tip cells, but it is not known how single tip cells are selected to lead each vessel sprout, and how tip-cell numbers are determined. Here we present evidence that delta-like 4 (Dll4)-Notch1 signalling regulates the formation of appropriate numbers of tip cells to control vessel sprouting and branching in the mouse retina. We show that inhibition of Notch signalling using gamma-secretase inhibitors, genetic inactivation of one allele of the endothelial Notch ligand Dll4, or endothelial-specific genetic deletion of Notch1, all promote increased numbers of tip cells. Conversely, activation of Notch by a soluble jagged1 peptide leads to fewer tip cells and vessel branches. Dll4 and reporters of Notch signalling are distributed in a mosaic pattern among endothelial cells of actively sprouting retinal vessels. At this location, Notch1-deleted endothelial cells preferentially assume tip-cell characteristics. Together, our results suggest that Dll4-Notch1 signalling between the endothelial cells within the angiogenic sprout serves to restrict tip-cell formation in response to VEGF, thereby establishing the adequate ratio between tip and stalk cells required for correct sprouting and branching patterns. This model offers an explanation for the dose-dependency and haploinsufficiency of the Dll4 gene, and indicates that modulators of Dll4 or Notch signalling, such as gamma-secretase inhibitors developed for Alzheimer's disease, might find usage as pharmacological regulators of angiogenesis.     

Direct observation of second-order atom tunnelling

Tunnelling of material particles through a classically impenetrable barrier constitutes one of the hallmark effects of quantum physics. When interactions between the particles compete with their mobility through a tunnel junction, intriguing dynamical behaviour can arise because the particles do not tunnel independently. In single-electron or Bloch transistors, for example, the tunnelling of an electron or Cooper pair can be enabled or suppressed by the presence of a second charge carrier due to Coulomb blockade. Here we report direct, time-resolved observations of the correlated tunnelling of two interacting ultracold atoms through a barrier in a double-well potential. For the regime in which the interactions between the atoms are weak and tunnel coupling dominates, individual atoms can tunnel independently, similar to the case of a normal Josephson junction. However, when strong repulsive interactions are present, two atoms located on one side of the barrier cannot separate, but are observed to tunnel together as a pair in a second-order co-tunnelling process. By recording both the atom position and phase coherence over time, we fully characterize the tunnelling process for a single atom as well as the correlated dynamics of a pair of atoms for weak and strong interactions. In addition, we identify a conditional tunnelling regime in which a single atom can only tunnel in the presence of a second particle, acting as a single atom switch. Such second-order tunnelling events, which are the dominating dynamical effect in the strongly interacting regime, have not been previously observed with ultracold atoms. Similar second-order processes form the basis of superexchange interactions between atoms on neighbouring lattice sites of a periodic potential, a central component of proposals for realizing quantum magnetism.     

Influence of the intertropical convergence zone on the East Asian monsoon

The Asian-Australian monsoon is an important component of the Earth's climate system that influences the societal and economic activity of roughly half the world's population. The past strength of the rain-bearing East Asian summer monsoon can be reconstructed with archives such as cave deposits, but the winter monsoon has no such signature in the hydrological cycle and has thus proved difficult to reconstruct. Here we present high-resolution records of the magnetic properties and the titanium content of the sediments of Lake Huguang Maar in coastal southeast China over the past 16,000 years, which we use as proxies for the strength of the winter monsoon winds. We find evidence for stronger winter monsoon winds before the B?lling-Aller?d warming, during the Younger Dryas episode and during the middle and late Holocene, when cave stalagmites suggest weaker summer monsoons. We conclude that this anticorrelation is best explained by migrations in the intertropical convergence zone. Similar migrations of the intertropical convergence zone have been observed in Central America for the period ad 700 to 900 (refs 4-6), suggesting global climatic changes at that time. From the coincidence in timing, we suggest that these migrations in the tropical rain belt could have contributed to the declines of both the Tang dynasty in China and the Classic Maya in Central America.     

Noninvasively diagnosing coronary artery disease with 61-channel MCG data

Magnetocardiography(MCG) has been investigated as a tool for noninvasive detection of coronary artery disease(CAD). In this study, the area ratio of positive and negative magnetic induction extracted from an extrema circle in the magnetocardiogram was analyzed at specific time points in the cardiac cycle: P maximum, R peak, J point, T onset, T peak and T end. The area of the positive proportion of the magnetic field relative to the total area within a circle encompassing the field extrema was determined and proposed for fast-speed CAD diagnosis. MCG was performed with a 61-channel biomagnetometer in a shielded environment in 38 healthy subjects and 15 CAD patients. A notable difference in area ratio was found between healthy and CAD subjects at the peak time of T wave: 0.416 ± 0.090 versus0.465 ± 0.065(p = 0.013). Using a cutoff value of 0.4506resulted in a sensitivity and specificity of 86.7 % and 73.8 %,respectively. This approach may enable a fast-speed CAD diagnosis in a clinical setting.     

Polymer光波导器件的电极分析

设计了以有机聚合物（Ｐｏｌｙｍ ｅｒ）作为光波导的电光调制器的电极．通过理论推导和计算机辅助数值计算得出电极的特征阻抗和导体损耗系数,以及它们与电极的宽度、高度、厚度之间的关系．分析了电极宽度、高度、厚度的变化对特征阻抗和导体损耗系数的影响,以及导体损耗对调制带宽的影响,并模拟了Ｐｏｌｙｍ ｅｒ光波导调制器的频率响应．通过频率响应曲线得知电极的极限带宽在１００ ＧＨｚ以上．     

Low density lipoprotein receptor-related protein 1 couples β1 integrin activation to degradation

Low density lipoprotein receptor-related protein (LRP) 1 modulates cell adhesion and motility under normal and pathological conditions. Previous studies documented that LRP1 binds several integrin receptors and mediates their trafficking to the cell surface and endocytosis. However, the mechanism by which LRP1 may regulate integrin activation remains unknown. Here we report that LRP1 promotes the activation and subsequent degradation of β1 integrin and thus supports cell adhesion, spreading, migration and integrin signaling on fibronectin. LRP1 interacts with surface β1 integrin, binds the integrin activator kindlin2 and stimulates β1 integrin–kindlin2 complex formation. Specifically, serine 76 in the LRP1 cytoplasmic tail is crucial for the interaction with kindlin2, β1 integrin activation and cell adhesion. Interestingly, a loss of LRP1 induces the accumulation of several integrin receptors on the cell surface. Following internalization, intracellular trafficking of integrins is driven by LRP1 in a protein kinase C- and class II myosin-dependent manner. Ultimately, LRP1 dictates the fate of endocytosed β1 integrin by directing it down the pathway of lysosomal and proteasomal degradation. We propose that LRP1 mediates cell adhesion by orchestrating a multi-protein pathway to activate, traffic and degrade integrins. Thus, LRP1 may serve as a focal point in the integrin quality control system to ensure a firm connection to the extracellular matrix.     

Phosphatidylinositol-3,5-bisphosphate lipid-binding-induced activation of the human two-pore channel 2

Mammalian two-pore channels (TPCs) are activated by the low-abundance membrane lipid phosphatidyl-(3,5)-bisphosphate (PI(3,5)P₂) present in the endo-lysosomal system. Malfunction of human TPC1 or TPC2 (hTPC) results in severe organellar storage diseases and membrane trafficking defects. Here, we compared the lipid-binding characteristics of hTPC2 and of the PI(3,5)P₂-insensitive TPC1 from the model plant Arabidopsis thaliana. Combination of simulations with functional analysis of channel mutants revealed the presence of an hTPC2-specific lipid-binding pocket mutually formed by two channel regions exposed to the cytosolic side of the membrane. We showed that PI(3,5)P₂ is simultaneously stabilized by positively charged amino acids (K203, K204, and K207) in the linker between transmembrane helices S4 and S5 and by S322 in the cytosolic extension of S6. We suggest that PI(3,5)P₂ cross links two parts of the channel, enabling their coordinated movement during channel gating.