X-ray absorption fine structure study on residue bromine in carbons with different degrees of graphitization

The structure of bromine residue compounds was investigated by X-ray absorption fine structure (XAFS) in order to interpret where and how bromine is present in carbons with different degrees of graphitization. The residue compounds can be classified into three groups, as obtained from X-ray absorption near edge structure (XANES) spectra and the values of the intramolecular distance r_Br–Br determined by extended X-ray absorption fine structure (EXAFS). In Group I, prepared from the host carbons heat treated at temperatures higher than 1900 °C, bromine exists in the interlayer space of graphite in the form of Br₂ molecules with interaction of the π electrons of graphite. In Group III, from carbon heat treated at 1000 °C, most of the bromine probably reacts with carbon atoms having a dangling bond or functional groups. For Group II, where the host carbons are heat treated at intermediate temperatures, it is likely that bromine exists in undeveloped defects with a unique electronic state.     

Study of step instability on Si surfaces

Step instabilities on Si(1 1 1) vicinal surface and Si(1 1 1) vicinal surface induced by Au adsorption were observed by reflection electron microscopy. On the Si(0 0 1) vicinal surface faceting of (0 0 1) surface due to surface reconstruction takes place and surface steps are bunching. The kinetics of mass transport of Si depends on the substrate temperature and steps are impermeable for Si adatoms at lower temperature and they are permeable at higher temperature. On the Si(1 1 1) vicinal surface the permeability of steps depends on the heating current direction. The steps are permeable for step-up current heating and are impermeable for step-down current heating. Above a critical coverage of Au (≈0.3 ML) steps are bunching irrespective of heating current direction and periodic array of extremely straight step bands is formed for the step-down current heating.     

Learning of real robot's inverse dynamics by a forward‐propagation learning rule

A forward‐propagation learning rule (FPL) has been proposed for a neural network (NN) to learn an inverse model of a controlled object. A feature of FPL is that the trajectory error propagates forward in NN and appropriate values of two learning parameters are required to be set. FPL has only been simulated to several kinds of controlled objects such as a two‐link arm in a horizontal plane. In this work, we applied FPL to AIBO and showed the validity of FPL on a real controlled object. At first, we tested a learning experiment of an inverse dynamic of a two‐link arm in a sagittal plane with viscosity and Coulomb friction by computer simulation. In this simulation, a low‐pass filter (LPF) was applied to realized trajectories because coulomb friction vibrates them. From the simulation results, we found that the learning process is stable by some adequate sets of the learning parameters although it is more sensitive to the values of the parameters owing to friction and gravity terms. Finally, we tested applying FPL to motor control of AIBO's leg. The inverse dynamics model was acquired by FPL with only about 150 learning iterations. From these results, the validity of the FPL was confirmed by the real robot control experiments. © 2007 Wiley Periodicals, Inc. Electr Eng Jpn, 161(4): 38–48, 2007; Published online in Wiley InterScience ( www.interscience.wiley.com ). DOI 10.1002/eej.20456     

A 60-GHz multilayer parasitic microstrip array antenna on LTCC substrate for system-on-package

This letter describes a compact and high-gain multilayer parasitic microstrip array antenna (MPMAA). The design and performance of the proposed array antenna are presented. The antenna employs three layers with a 2/spl times/2 parasitic array on each layer. The developed prototype MPMAA employs a multilayer low-temperature co-fired ceramic (LTCC) substrate that is well suited to the assembly of MMIC chips. The fabricated MPMAA achieves a 7.17 dBi absolute gain at 60 GHz including the loss derived from the feeding parts and RF probe to measure its antenna performance. The spacing of the top layer of the parasitic array constructed by 2/spl times/2 elements has a free-space wavelength of 0.36 and the chip size is 10 mm/sup 2/. The fabricated MPMAA achieves both compact and high directional gain and satisfies the requirements for a millimeter-wave system-on-package (SOP).     

T cell response to Borrelia garinii, Borrelia afzelii, and Borrelia japonica in various congenic mouse strains

The infectivity and T cell response to Borrelia garinii SIKA2, Borrelia afzelii BFOX, and Borrelia japonica 0612, the organisms that cause Lyme disease in Japan, were examined in various inbred and congenic strains of mice. Infectivity differed among the species: B. garinii SIKA2 and B. afzelii BFOX were each able to infect 90% to 100% of C3H/He mice; B. japonica 0612 was able to infect only 20% of C3H/He mice. The pattern of infectivity to various inbred and congenic strains of mice may influence the pathogenicity of the organism and the clinical signs of Lyme disease. Cross-reactivity between Borrelia antigens was observed, but there was no cross-reactivity between Borrelia antigens and Leptospira antigens. We evaluated the genetic control of the delayed-type hypersensitivity (DTH) reaction in the form of footpad swelling produced by Borrelia antigens using viable or sonicated bacteria as sensitization. Differences in strains of mice infected by viable antigen were observed. However, all strains of mice showed a strong DTH reaction using sonicated antigens without genetic background. A DTH reaction in the form of footpad swelling did not appear to be associated with genetic background. The footpad reaction was mediated by CD4+8- and Ia- T cells, as revealed by in vitro monoclonal antibody treatment. However, CD8+ T cells did not suppress footpad swelling. These results indicate that many antigenic epitopes of the Borrelia spirochete can stimulate the DTH reaction.     

New hot-carrier degradation mode in PMOSFETs with W gate electrodes

Hot-carrier degradation of W gate PMOSFETs, which are surface-channel devices because of the work function of W, has been investigated in comparison with polycide (WSi_x/n⁺ poly-Si) ones. In W gate PMOSFETs, transconductance g_m and threshold voltage V_th decrease on the drain avalanche hot-carrier (DAHC) stress, and Δg_m /g_m0 and ΔV_th become minimum at V_G≅V_D/2. By using the charge-pumping technique, it is found that, after stressing at the same stress condition, the interface state density of W gate devices is about 10 times larger than that of polycide ones but the densities of trapped electrons are almost equal. These results indicate that the difference of hot-carrier degradation between W and polycide gate devices is mainly caused by the difference of the interface state density     

Effects of monoclonal anti-c-kit antibody (ACK2) on melanocytes in newborn mice

Previous studies indicate that c-Kit is required for postnatal melanocyte development. To understand the precise mechanisms of c-Kit dependence, we studied melanocyte development in newborn C57BL/6 mice by means of peritoneal injection of a monoclonal anti-c-Kit antibody (ACK2), which blocks c-Kit functions. The mice were injected once or more with ACK2 at various intervals after birth. In experiment 1, skin samples were examined on day 10 post-partum and in experiment 2 they were examined daily until day 10 post-partum. We studied melanocytes in the hair follicles, epidermis, and dermis by light and electron microscopy with dopa reactions and immunohistochemistry. Epidermal melanocytes in untreated mice were dopa negative and c-Kit positive on day 0 post-partum but became dopa positive soon thereafter. In ACK2-treated mice, the earlier the mice received ACK2 injections after birth, the fewer melanocytes they had, not only in the epidermis, but also in follicles. In these mice, melanocytes that had undergone apoptosis in the dermis and the follicles were detected ultrastructurally. Some appeared to have produced tyrosinase, because they had dopa-positive melanosomes. These results suggest that melanocytes in newborn mice are c-Kit dependent and undergo apoptosis when c-Kit receptors are blocked by ACK2 in the early days after birth. During this c-Kit-dependent period, melanocytes differentiate from dopa negative to positive and migrate from the epidermis to hair follicles.     

A defect in GTP synthesis affects mannose outer chain elongation in Saccharomyces cerevisiae

Clonal central nervous system neuronal cells, B103, do not synthesize detectable endogenous APP or APLP. B103 cells transfected with both wild-type (B103/APP) and mutant APP construct (B103/APP delta NL) secreted comparable amounts of soluble forms of APP (sAPP). B103/APP cells produced sAPP and cleaved at amyloid beta/A4 (A beta) 16, the alpha-secretase site, and B103/APP delta NL cells produced sAPP beta cleaved at A beta 1, the beta-secretase site. B103/APP delta NL cells developed fewer neurites than B103/APP cells in a serum-free defined medium. Neurite numbers of parent B103 cells were increased by the 50% conditioned medium (CM) from B103/APP cells but reduced by the CM from B103/APP delta NL cells. Chemically synthesized A beta at concentration levels higher than 1 nM reduced numbers of neurites from B103 or B103/APP delta NL cells. However, A beta at 1-100 nM could not reduce the neurite number of B103/APP cells. The protective activity against A beta's deleterious effect to reduce neurite numbers was attributed to sAPP alpha in the CM. Although sAPP alpha could block the effect of A beta, sAPP beta could not do so under the identical condition, suggesting the importance of the C-terminal 15-amino acid sequence in sAPP alpha. Nevertheless, sAPP alpha's protective activity required the N-terminal sequence around RERMS, previously identified to be the active domain of sAPP beta. The overall effect of APP mutation which overproduced A beta and sAPP beta and underproduced sAPP alpha was a marked decline in the neurotrophic effect of APP. We suggest that the disruption of balance between the detrimental effect of A beta and the trophic effect of sAPP may be important in the pathogenesis of AD caused by this pathogenic APP mutation.