Synthesis of carbon-nitride films using a fast-switched dual-source low energy ion beam deposition system

Thin C_xN_y films were deposited in UHV using alternating low energy ion beams of C⁺ and N⁺ or N₂⁺ in the energy range of 5 to 100 eV. The ion beam deposition system is equipped with two Freeman ion sources, mass analysis and fast automated beam switching, allowing perpendicular bombardment of the target with a single ion beam at a time. The composition and density of the films were studied by ARS (in situ), XPS and RBS. The dependence of the film properties and growth mechanisms on ion energy, beam switching rate, and C-to-N arrival ratio have been investigated. The influence of the deposition parameters on the film stoichiometry is discussed. Exposure of the film to atmosphere leads to oxygen incorporation, resulting in a lowered surface concentration of nitrogen. The XPS N 1s and C Is binding energies vary in a relatively broad range indicating that several bond states may be present. The influence of the substrate material on film growth has also been studied. On Si{100}, film growth commences with the formation of an interfacial silicon nitride. No film growth was observed on gold, however deposition was possible on tantalum and molybdenum.     

From task parameters to motor synergies: A hierarchical framework for approximately optimal control of redundant manipulators

We present a hierarchical framework for approximately optimal control of redundant manipulators. The plant is augmented with a low‐level feedback controller, designed to yield input‐output behavior that captures the task‐relevant aspects of plant dynamics but has reduced dimensionality. This makes it possible to reformulate the optimal control problem in terms of the augmented dynamics, and optimize a high‐level feedback controller without running into the curse of dimensionality. The resulting control hierarchy compares favorably to existing methods in robotics. Furthermore, we demonstrate a number of similarities to (nonhierarchical) optimal feedback control. Besides its engineering applications, the new framework addresses a key unresolved problem in the neural control of movement. It has long been hypothesized that coordination involves selective control of task parameters via muscle synergies, but the link between these parameters and the synergies capable of controlling them has remained elusive. Our framework provides this missing link. © 2005 Wiley Periodicals, Inc.     

Collision dynamics of elliptically polarized solitons in Coupled Nonlinear Schrödinger Equations

We investigate numerically the collision dynamics of elliptically polarized solitons of the System of Coupled Nonlinear Schrödinger Equations (SCNLSE) for various different initial polarizations and phases. General initial elliptic polarizations (not sech$sech$-shape) include as particular cases the circular and linear polarizations. The elliptically polarized solitons are computed by a separate numerical algorithm. We find that, depending on the initial phases of the solitons, the polarizations of the system of solitons after the collision change, even for trivial cross-modulation. This sets the limits of practical validity of the celebrated Manakov solution. For general nontrivial cross-modulation, a jump in the polarization angles of the solitons takes place after the collision (‘polarization shock’). We study in detail the effect of the initial phases of the solitons and uncover different scenarios of the quasi-particle behavior of the solution. In majority of cases the solitons survive the interaction preserving approximately their phase speeds and the main effect is the change of polarization. However, in some intervals for the initial phase difference, the interaction is ostensibly inelastic: either one of the solitons virtually disappears, or additional solitons are born after the interaction. This outlines the role of the phase, which has not been extensively investigated in the literature until now.     

Human brain metabolic response to caffeine and the effects of tolerance

OBJECTIVE: Since there is limited information concerning caffeine's metabolic effects on the human brain, the authors applied a rapid proton echo-planar spectroscopic imaging technique to dynamically measure regional brain metabolic responses to caffeine ingestion. They specifically measured changes in brain lactate due to the combined effects of caffeine's stimulation of glycolysis and reduction of cerebral blood flow. METHOD: Nine heavy caffeine users and nine caffeine-intolerant individuals, who had previously discontinued or substantially curtailed use of caffeinated products because of associated anxiety and discomforting physiological arousal, were studied at baseline and then during 1 hour following ingestion of caffeine citrate (10 mg/kg). To assess state-trait contributions and the effects of caffeine tolerance, five of the caffeine users were restudied after a 1- to 2-month caffeine holiday. RESULTS: The caffeine-intolerant individuals, but not the regular caffeine users, experienced substantial psychological and physiological distress in response to caffeine ingestion. Significant increases in global and regionally specific brain lactate were observed only among the caffeine-intolerant subjects. Reexposure of the regular caffeine users to caffeine after a caffeine holiday resulted in little or no adverse clinical reaction but significant rises in brain lactate which were of a magnitude similar to that observed for the caffeine-intolerant group. CONCLUSIONS: These results provide direct evidence for the loss of caffeine tolerance in the human brain subsequent to caffeine discontinuation and suggest mechanisms for the phenomenon of caffeine intolerance other than its metabolic effects on elevating brain lactate.     

Mercuric chloride induces increases in both cytoplasmic and nuclear free calcium ions through a protein phosphorylation-linked mechanism

The mechanism of the lymphocyte stimulatory action of sulfhydryl group-reactive mercuric ions was studied with respect to its potential ability to induce a protein tyrosine phosphorylation-linked signal for mobilization of free Ca2+ into cytoplasm and nucleus of the cell. Exposure of human leukamic T cell line (Jurkat) cells to high (1 mM) and low (0.01 mM) concentrations of HgCl2 induced tyrosine phosphorylation of multiple proteins in a concentration-dependent manner. Confocal microscopy directly visualized the time course localization of Ca2+ inside the cells after exposure to HgCl2. The onset and level of Ca2+ mobilization following HgCl2 exposure were in parallel to those of protein tyrosine phosphorylation. Interestingly, by either concentration of HgCl2, Ca2+ was mobilized in both cytoplasm and nucleus almost simultaneously, and the level of Ca2+ mobilization in the nucleus was more than that in the cytoplasm. All the HgCl2-mediated Ca2+ mobilization was prevented by addition of protein kinase inhibitor staurosporin prior to HgCl2. These results suggest that heavy metal stress triggers a protein tyrosine phosphorylation-linked signal that leads to a nuclear event-dominant Ca2+ mobilization.     

Identification of 130 kDa cell surface LDL-binding protein from smooth muscle cells as a partially processed T-cadherin precursor

Atypical cell surface lipoprotein-binding proteins of 105 kDa and 130 kDa are present in membranes of vascular smooth muscle cells. We recently identified the 105 kDa protein from human aortic media as T-cadherin, an unusual glycosylphosphatidylinositol (GPI)-anchored member of the cadherin family of cell adhesion proteins. The goal of the present study was to determine the identity of 130 kDa lipoprotein-binding protein of smooth muscle cells. We applied different approaches that included protein sequencing of purified protein from human aortic media, the use of human T-cadherin peptide-specific antisera, and enzymatic treatment of cultured cells with trypsin and GPI-specific phospholipase C. Our results indicate that the 130 kDa protein is a partially processed form of T-cadherin which is attached to the membrane surface of smooth muscle cells via a GPI anchor and contains uncleaved N-terminal propeptide sequence. Our data disclose that, in contrast to classical cadherins, T-cadherin is expressed on the cell surface in both its precursor (130 kDa) and mature (105 kDa) forms.     

Modulation of (+/-)-anti-BPDE mediated p53 accumulation by inhibitors of protein kinase C and poly(ADP-ribose) polymerase

The rapid accumulation of the p53 gene product is considered to be an important component of the cellular response to a variety of genotoxins. In order to gain insights on the biochemical pathways leading to p53 stabilization, the effect of (+/-) 7,8-dihydroxy-anti-9, 10-epoxy-7,8,9,10-tetrahydrobenzo(a)-pyrene [(+/-)-anti-BPDE] induced DNA damage on p53 protein levels was investigated in various repair-proficient and repair-deficient human cells. Brief exposure of normal human fibroblasts to 0.05-1 microM (+/-)-anti-BPDE resulted in elevated p53 protein levels as compared to the constitutive levels of control cells. The rapid induction response, detectable within a few hours, was sustained up to a period of at least 24 h. Repair-proficient and repair-deficient (XPA) human lymphoblastoid cells showed a similar response. The poly(ADP-ribose) polymerase inhibitor, 3-aminobenzamide (3-AB), diminished the p53 induction response by concomitantly decreasing the extent of (+/-)-anti-BPDE induced DNA damage in cells pretreated with the inhibitor. However, the direct involvement of poly ADP-ribosylation was also apparent as 3-AB was able to attenuate (approximately 50%) the p53 response by post-damage inhibitor treatment of the cells. Inhibition of cellular DNA replication by hydroxyurea and AraC, in the presence or absence of DNA damage, also resulted in rapid p53 accumulation in repair-deficient cells. On the contrary, inhibition of protein kinase C (PKC) by calphostin-C led to an abrogation of (+/-)-anti-BPDE mediated p53 induction. Analysis of the downstream effects of carcinogen treatment showed that the lymphoblastoid cells undergo DNA fragmentation indicative of apoptosis while fibroblasts exhibit cell cycle arrest at the G1-S boundary.