A review of three species of Hesperonoe (Annelida: Polynoidae) in Asia,with descriptions of two new species and a new record of Hesperonoe hwanghaiensis from Korea

A taxonomic review of three Asian species of Hesperonoe (Annelida: Polynoidae) is presented. Hesperonoe hwanghaiensis Uschakov and Wu, 1959 Uschakov PV, Wu B. 1959. [The polychaete worms of the families Phyllodocidae and Aphroditidae (Polychaeta, errantia) from the Yellow Sea]. Arch Inst Oceanol Sinica. 1:1–40, pls. I–X. (In Chinese and Russian). [Google Scholar] (type locality: Qingdao, China) is redescribed based on five specimens collected from an intertidal site in the Korean coast of the Yellow Sea, as a new record of this species from Korea, which is the only known habitat outside the type locality. Hesperonoe coreensis sp. nov. is described based on nine specimens collected from two intertidal sites in the Korean coast of the Yellow Sea, including the same site as the habitat of H. hwanghaiensis. Hesperonoe japonensis sp. nov. is described by re-examination of many specimens collected from eight intertidal sites and a subtidal one in Japan, which was previously misidentified as H. hwanghaiensis. The three species are clearly distinguishable from one another by the species-specific morphology of the macrotubercles (or marked ridges) on the surface of elytra. All of the three species seemed to be commensal with the burrowing mud shrimp Upogebia major in intertidal flats, except for an additional probable host of another upogebid shrimp Austinogebia narutensis for H. japonensis sp. nov. in a subtidal habitat. The morphological characteristics and host species of the three Asian species are compared with all of the other five congeners known from the North American Pacific and Arctic Sea.

http://www.zoobank.org/urn:lsid:zoobank.org:pub:51CB5C5B-0838-48AC-A0BA-8E63AA7628CB     

Atom-by-atom spectroscopy at graphene edge

The properties of many nanoscale devices are sensitive to local atomic configurations, and so elemental identification and electronic state analysis at the scale of individual atoms is becoming increasingly important. For example, graphene is regarded as a promising candidate for future devices, and the electronic properties of nanodevices constructed from this material are in large part governed by the edge structures. The atomic configurations at graphene boundaries have been investigated by transmission electron microscopy and scanning tunnelling microscopy, but the electronic properties of these edge states have not yet been determined with atomic resolution. Whereas simple elemental analysis at the level of single atoms can now be achieved by means of annular dark field imaging or electron energy-loss spectroscopy, obtaining fine-structure spectroscopic information about individual light atoms such as those of carbon has been hampered by a combination of extremely weak signals and specimen damage by the electron beam. Here we overcome these difficulties to demonstrate site-specific single-atom spectroscopy at a graphene boundary, enabling direct investigation of the electronic and bonding structures of the edge atoms-in particular, discrimination of single-, double- and triple-coordinated carbon atoms is achieved with atomic resolution. By demonstrating how rich chemical information can be obtained from single atoms through energy-loss near-edge fine-structure analysis, our results should open the way to exploring the local electronic structures of various nanodevices and individual molecules.     

Structural basis for semaphorin signalling through the plexin receptor

Semaphorins and their receptor plexins constitute a pleiotropic cell-signalling system that is used in a wide variety of biological processes, and both protein families have been implicated in numerous human diseases. The binding of soluble or membrane-anchored semaphorins to the membrane-distal region of the plexin ectodomain activates plexin's intrinsic GTPase-activating protein (GAP) at the cytoplasmic region, ultimately modulating cellular adhesion behaviour. However, the structural mechanism underlying the receptor activation remains largely unknown. Here we report the crystal structures of the semaphorin 6A (Sema6A) receptor-binding fragment and the plexin A2 (PlxnA2) ligand-binding fragment in both their pre-signalling (that is, before binding) and signalling (after complex formation) states. Before binding, the Sema6A ectodomain was in the expected 'face-to-face' homodimer arrangement, similar to that adopted by Sema3A and Sema4D, whereas PlxnA2 was in an unexpected 'head-on' homodimer arrangement. In contrast, the structure of the Sema6A-PlxnA2 signalling complex revealed a 2:2 heterotetramer in which the two PlxnA2 monomers dissociated from one another and docked onto the top face of the Sema6A homodimer using the same interface as the head-on homodimer, indicating that plexins undergo 'partner exchange'. Cell-based activity measurements using mutant ligands/receptors confirmed that the Sema6A face-to-face dimer arrangement is physiologically relevant and is maintained throughout signalling events. Thus, homodimer-to-heterodimer transitions of cell-surface plexin that result in a specific orientation of its molecular axis relative to the membrane may constitute the structural mechanism by which the ligand-binding 'signal' is transmitted to the cytoplasmic region, inducing GAP domain rearrangements and activation.     

Identification of Tim4 as a phosphatidylserine receptor

In programmed cell death, a large number of cells undergo apoptosis, and are engulfed by macrophages to avoid the release of noxious materials from the dying cells. In definitive erythropoiesis, nuclei are expelled from erythroid precursor cells and are engulfed by macrophages. Phosphatidylserine is exposed on the surface of apoptotic cells and on the nuclei expelled from erythroid precursor cells; it works as an 'eat me' signal for phagocytes. Phosphatidylserine is also expressed on the surface of exosomes involved in intercellular signalling. Here we established a library of hamster monoclonal antibodies against mouse peritoneal macrophages, and found an antibody that strongly inhibited the phosphatidylserine-dependent engulfment of apoptotic cells. The antigen recognized by the antibody was identified by expression cloning as a type I transmembrane protein called Tim4 (T-cell immunoglobulin- and mucin-domain-containing molecule; also known as Timd4). Tim4 was expressed in Mac1+ cells in various mouse tissues, including spleen, lymph nodes and fetal liver. Tim4 bound apoptotic cells by recognizing phosphatidylserine via its immunoglobulin domain. The expression of Tim4 in fibroblasts enhanced their ability to engulf apoptotic cells. When the anti-Tim4 monoclonal antibody was administered into mice, the engulfment of apoptotic cells by thymic macrophages was significantly blocked, and the mice developed autoantibodies. Among the other Tim family members, Tim1, but neither Tim2 nor Tim3, specifically bound phosphatidylserine. Tim1- or Tim4-expressing Ba/F3 B cells were bound by exosomes via phosphatidylserine, and exosomes stimulated the interaction between Tim1 and Tim4. These results indicate that Tim4 and Tim1 are phosphatidylserine receptors for the engulfment of apoptotic cells, and may also be involved in intercellular signalling in which exosomes are involved.     

Helicobacter pylori CagA targets PAR1/MARK kinase to disrupt epithelial cell polarity

Helicobacter pylori cagA-positive strains are associated with gastritis, ulcerations and gastric adenocarcinoma. CagA is delivered into gastric epithelial cells and, on tyrosine phosphorylation, specifically binds and activates the SHP2 oncoprotein, thereby inducing the formation of an elongated cell shape known as the 'hummingbird' phenotype. In polarized epithelial cells, CagA also disrupts the tight junction and causes loss of apical-basolateral polarity. We show here that H. pylori CagA specifically interacts with PAR1/MARK kinase, which has an essential role in epithelial cell polarity. Association of CagA inhibits PAR1 kinase activity and prevents atypical protein kinase C (aPKC)-mediated PAR1 phosphorylation, which dissociates PAR1 from the membrane, collectively causing junctional and polarity defects. Because of the multimeric nature of PAR1 (ref. 14), PAR1 also promotes CagA multimerization, which stabilizes the CagA-SHP2 interaction. Furthermore, induction of the hummingbird phenotype by CagA-activated SHP2 requires simultaneous inhibition of PAR1 kinase activity by CagA. Thus, the CagA-PAR1 interaction not only elicits the junctional and polarity defects but also promotes the morphogenetic activity of CagA. Our findings revealed that PAR1 is a key target of H. pylori CagA in the disorganization of gastric epithelial architecture underlying mucosal damage, inflammation and carcinogenesis.     

p53-induced inhibition of Hif-1 causes cardiac dysfunction during pressure overload

Cardiac hypertrophy occurs as an adaptive response to increased workload to maintain cardiac function. However, prolonged cardiac hypertrophy causes heart failure, and its mechanisms are largely unknown. Here we show that cardiac angiogenesis is crucially involved in the adaptive mechanism of cardiac hypertrophy and that p53 accumulation is essential for the transition from cardiac hypertrophy to heart failure. Pressure overload initially promoted vascular growth in the heart by hypoxia-inducible factor-1 (Hif-1)-dependent induction of angiogenic factors, and inhibition of angiogenesis prevented the development of cardiac hypertrophy and induced systolic dysfunction. Sustained pressure overload induced an accumulation of p53 that inhibited Hif-1 activity and thereby impaired cardiac angiogenesis and systolic function. Conversely, promoting cardiac angiogenesis by introducing angiogenic factors or by inhibiting p53 accumulation developed hypertrophy further and restored cardiac dysfunction under chronic pressure overload. These results indicate that the anti-angiogenic property of p53 may have a crucial function in the transition from cardiac hypertrophy to heart failure.     

Tbx6-dependent Sox2 regulation determines neural or mesodermal fate in axial stem cells

The classical view of neural plate development held that it arises from the ectoderm, after its separation from the mesodermal and endodermal lineages. However, recent cell-lineage-tracing experiments indicate that the caudal neural plate and paraxial mesoderm are generated from common bipotential axial stem cells originating from the caudal lateral epiblast. Tbx6 null mutant mouse embryos which produce ectopic neural tubes at the expense of paraxial mesoderm must provide a clue to the regulatory mechanism underlying this neural versus mesodermal fate choice. Here we demonstrate that Tbx6-dependent regulation of Sox2 determines the fate of axial stem cells. In wild-type embryos, enhancer N1 of the neural primordial gene Sox2 is activated in the caudal lateral epiblast, and the cells staying in the superficial layer sustain N1 activity and activate Sox2 expression in the neural plate. In contrast, the cells destined to become mesoderm activate Tbx6 and turn off enhancer N1 before migrating into the paraxial mesoderm compartment. In Tbx6 mutant embryos, however, enhancer N1 activity persists in the paraxial mesoderm compartment, eliciting ectopic Sox2 activation and transforming the paraxial mesoderm into neural tubes. An enhancer-N1-specific deletion mutation introduced into Tbx6 mutant embryos prevented this Sox2 activation in the mesodermal compartment and subsequent development of ectopic neural tubes, indicating that Tbx6 regulates Sox2 via enhancer N1. Tbx6-dependent repression of Wnt3a in the paraxial mesodermal compartment is implicated in this regulatory process. Paraxial mesoderm-specific misexpression of a Sox2 transgene in wild-type embryos resulted in ectopic neural tube development. Thus, Tbx6 represses Sox2 by inactivating enhancer N1 to inhibit neural development, and this is an essential step for the specification of paraxial mesoderm from the axial stem cells.     

气体绝缘系统电极表面覆膜时金属导电微粒带电原因分析

在施加直流或交流电压的表面覆涂绝缘介质的楔形电极结构条件下，讨论了SF6中自由金属导电微粒在电场梯度力存在时的运动特性．通过实验测得的自由导电微粒运动起始时的电压，计算得到微粒所带电荷量，该结果与采用法拉第筒测得的结果吻合，即当电极表面覆以100μm厚的聚对苯二甲酸乙二醇酯(PET)薄膜时，微粒带电量约为未覆膜时的30％～60％．通过对微粒与介质间局部放电导致发光现象的实验观测研究，表明表面覆涂绝缘介质的非平行平板电极间自由金属导电微粒的带电机理在直流电压下为电导电流或薄膜表面极化带电，交流电压下为微粒与介质间的微放电．     

电火花线切割机加工自由曲面的CAD/CAM软件

用电火花线切割机加工自由曲面时,常规的NC编程无法精确、实时地调整电极丝与工件的相对位置。为此设计了一种CAD/CAM软件,该软件可依据被加工曲面的CAD数据,计算出加工点处电极丝的位置和姿态,并且根据加工点的法线矢量和电极丝的轴心矢量的交叉乘积决定加工点的移动方向,然后自动生成NC指令进行自由曲面的加工。利用这套软件对球面进行了加工实验。结果表明:加工得到的球面与仿真结果基本相似,加工精度取决于放电间隙及切向进给方式。