Prediction of grain structure in direct-chill cast Al–Zn–Mg–Cu billets using cellular automaton-finite element method

A cellular automaton-finite element (CA-FE) model was used to predict the solidification grain structure of permanent mold cast A7086 alloy. In this model, a Gaussian distribution of nucleation sites was adopted, and the Kurz-Giovanola-Trivedi model was extended to a multicomponent Al–Zn–Mg–Cu alloy system to determine the growth kinetics of the dendrite tip. For describing the Gaussian distribution of nucleation sites on the mold surface, an empirical relationship between the initial cooling rate of the melt and the nucleation density was proposed. Under various casting conditions, the calculated grain structures agreed well with the experimental results. Subsequently, the model was applied to the direct-chill (DC) cast billets, and the simulated grain structures reproduced well the experimental results. This confirmed that the current CA-FE model can be used practically and effectively in DC casting processes.     

Rational design of carbon shell-encapsulated cobalt nanospheres to enhance microwave absorption performance

Co@C core–shell nanospheres highly dispersed on carbon supports were rationally designed to improve the microwave absorbing property of the composite material, and fabricated by one pot thermal decomposition and simple annealing process. The Co nanospheres were completely encapsulated with thin carbon shells, which can effectively prevent the oxidation of the Co surface. Additionally, the particle size of Co nanospheres were properly controlled to optimize the electromagnetic property of the composite material. As a result, the lightweight Co@C/C composites with the particle size of 20 nm exhibited much enhanced microwave absorption properties. The improved microwave absorption performance is attributed mainly to the enhanced isotropic ratio and impedance matching of magnetic composites via tuning the Co particle size. Therefore, the welldesigned core-shell Co@C composite structure will provide a new insight for the development of high performance microwave absorbers.     

神经网络配合声发射传感器在钻岩和磨矿中的应用

该项研究是对声发射传感器联机探测岩石性质进行评价。首先探讨了声发射与岩石破碎机理的关系，然后介绍了把声发射传感器联接到锚杆孔钻机上，用反向传播神经网络“识别”岩石破碎特性和岩石种类。辨认岩石的准确度为９９％。试验表明，神经网络的计算和校准能力能够使声发射传感器发挥更佳的探测作用。     

Allele-specific motifs revealed by sequencing of self-peptides eluted from MHC molecules.

The crystal structures of major histocompatibility complex (MHC) molecules contain a groove occupied by heterogeneous material thought to represent peptides central to immune recognition, although until now relatively little characterization of the peptides has been possible. Exact information about the contents of MHC grooves is now provided. Moreover, each MHC class I allele has its individual rules to which peptides presented in the groove adhere.     

Isolation and analysis of naturally processed viral peptides as recognized by cytotoxic T cells.

Virus-infected cells can be eliminated by cytotoxic T lymphocytes (CTL), which recognize virus-derived peptides bound to major histocompatibility complex (MHC) class I molecules on the cell surface. Until now, this notion has relied on overwhelming but indirect evidence, as the existence of naturally processed viral peptides has not been previously reported. Here we show that such peptides can be extracted from virus-infected cells by acid elution. Both the naturally processed H-2-Db-restricted and H-2-Kd-restricted peptides from influenza nucleoprotein are smaller than the corresponding synthetic peptides, which have first been used to determine the respective CTL epitopes. As with minor histocompatibility antigens, occurrence of viral peptides seems to be heavily dependent on MHC class I molecules, because infected H-2d cells do not contain the H-2-Db-restricted peptide, and infected H-2b cells do not contain the H-2-Kd-restricted peptide. Our data provide direct experimental proof for the above notion on MHC-associated viral peptides on virus-infected cells.     

Reductive evolution suggested from the complete genome sequence of a plant-pathogenic phytoplasma

The minimal gene set essential for life has long been sought. We report the 860-kb genome of the obligate intracellular plant pathogen phytoplasma (Candidatus Phytoplasma asteris, OY strain). The phytoplasma genome encodes even fewer metabolic functions than do mycoplasma genomes. It lacks the pentose phosphate cycle and, more unexpectedly, ATP-synthase subunits, which are thought to be essential for life. This may be the result of reductive evolution as a consequence of life as an intracellular parasite in a nutrient-rich environment.     

TRIM25 RING-finger E3 ubiquitin ligase is essential for RIG-I-mediated antiviral activity

Retinoic-acid-inducible gene-I (RIG-I; also called DDX58) is a cytosolic viral RNA receptor that interacts with MAVS (also called VISA, IPS-1 or Cardif) to induce type I interferon-mediated host protective innate immunity against viral infection. Furthermore, members of the tripartite motif (TRIM) protein family, which contain a cluster of a RING-finger domain, a B box/coiled-coil domain and a SPRY domain, are involved in various cellular processes, including cell proliferation and antiviral activity. Here we report that the amino-terminal caspase recruitment domains (CARDs) of RIG-I undergo robust ubiquitination induced by TRIM25 in mammalian cells. The carboxy-terminal SPRY domain of TRIM25 interacts with the N-terminal CARDs of RIG-I; this interaction effectively delivers the Lys 63-linked ubiquitin moiety to the N-terminal CARDs of RIG-I, resulting in a marked increase in RIG-I downstream signalling activity. The Lys 172 residue of RIG-I is critical for efficient TRIM25-mediated ubiquitination and for MAVS binding, as well as the ability of RIG-I to induce antiviral signal transduction. Furthermore, gene targeting demonstrates that TRIM25 is essential not only for RIG-I ubiquitination but also for RIG-I-mediated interferon- production and antiviral activity in response to RNA virus infection. Thus, we demonstrate that TRIM25 E3 ubiquitin ligase induces the Lys 63-linked ubiquitination of RIG-I, which is crucial for the cytosolic RIG-I signalling pathway to elicit host antiviral innate immunity.