Growth mechanism and diffusion barrier property of plasma-enhanced atomic layer deposition Ti-Si-N thin films

Ti-Si-N thin films were deposited by plasma-enhanced atomic layer deposition from TiCl4, SiH4, and N-2/H-2/Ar plasma at 350 degrees C. For comparison, TiN plasma-enhanced atomic layer deposition (PEALD) was also performed from TiCl4. The effects of growth parameters on film properties were studied. Especially, the changes in sequences of precursor-reactant exposure steps were found to produce large change in the growth rates and Si concentration in the films. The results are discussed based upon the molecule-surface reaction mechanisms. Also, the Cu diffusion barrier properties of the PEALD Ti-Si-N films were investigated. PEALD Ti-Si-N films have shown better diffusion barrier properties than PEALD TiN films and can be a promising candidate for future Cu interconnect technology beyond 65 nm technology node.] (c) 2006 American Vacuum Society.open111513sciescopu

Quantum Oscillation Signatures of Pressure-induced Topological Phase Transition in BiTeI

We report the pressure-induced topological quantum phase transition of BiTeI single crystals using Shubnikov-de Haas oscillations of bulk Fermi surfaces. The sizes of the inner and the outer FSs of the Rashba-split bands exhibit opposite pressure dependence up to P=3.35 GPa, indicating pressure-tunable Rashba effect. Above a critical pressure P similar to 2 GPa, the Shubnikov-de Haas frequency for the inner Fermi surface increases unusually with pressure, and the Shubnikov-de Haas oscillations for the outer Fermi surface shows an abrupt phase shift. In comparison with band structure calculations, we find that these unusual behaviors originate from the Fermi surface shape change due to pressure-induced band inversion. These results clearly demonstrate that the topological quantum phase transition is intimately tied to the shape of bulk Fermi surfaces enclosing the time-reversal invariant momenta with band inversion.11117Ysciescopu

Genetic Comparison of Stemness of Human Umbilical Cord and Dental Pulp

published_or_final_versio

Multi-dimensional TOF-SIMS analysis for effective profiling of disease-related ions from the tissue surface

Time-of-flight secondary ion mass spectrometry (TOF-SIMS) emerges as a promising tool to identify the ions (small molecules) indicative of disease states from the surface of patient tissues. In TOF-SIMS analysis, an enhanced ionization of surface molecules is critical to increase the number of detected ions. Several methods have been developed to enhance ionization capability. However, how these methods improve identification of disease-related ions has not been systematically explored. Here, we present a multi-dimensional SIMS (MD-SIMS) that combines conventional TOF-SIMS and metal-assisted SIMS (MetA-SIMS). Using this approach, we analyzed cancer and adjacent normal tissues first by TOF-SIMS and subsequently by MetA-SIMS. In total, TOF- and MetA-SIMS detected 632 and 959 ions, respectively. Among them, 426 were commonly detected by both methods, while 206 and 533 were detected uniquely by TOF- and MetA-SIMS, respectively. Of the 426 commonly detected ions, 250 increased in their intensities by MetA-SIMS, whereas 176 decreased. The integrated analysis of the ions detected by the two methods resulted in an increased number of discriminatory ions leading to an enhanced separation between cancer and normal tissues. Therefore, the results show that MD-SIMS can be a useful approach to provide a comprehensive list of discriminatory ions indicative of disease states.1178Ysciescopu

Optical property and Stokes' shift of Zn <inf>1-x</inf>Cd <inf>x</inf>O thin films depending on Cd content

Ternary Zn1-x Cdx O films were grown on (0001) sapphire substrates by pulsed laser deposition. The energy band gap of Zn1-x Cdx O films decreases with increasing Cd content. An increase of Cd content also leads to the emission broadening, absorption edge broadening, and crystallinity degradation. The absorption edge and ultraviolet emission energy shift to lower energy from 3.357 eV to 3.295 eV and 3.338 eV to 3.157 eV, respectively, with increasing Cd content from 0.3% to 3% at 4 K. The Stokes' shift between the absorption and emission is observed and that indicates the increase of exciton localization with Cd content. © 2006 American Institute of Physics

Online algorithms for covering and packing problems with convex objectives

We present online algorithms for covering and packing problems with (non-linear) convex objectives. The convex covering problem is defined as ...postprin

Upregulation of the cell-cycle regulator RGC-32 in Epstein-Barr virus-immortalized cells

Epstein-Barr virus (EBV) is implicated in the pathogenesis of multiple human tumours of lymphoid and epithelial origin. The virus infects and immortalizes B cells establishing a persistent latent infection characterized by varying patterns of EBV latent gene expression (latency 0, I, II and III). The CDK1 activator, Response Gene to Complement-32 (RGC-32, C13ORF15), is overexpressed in colon, breast and ovarian cancer tissues and we have detected selective high-level RGC-32 protein expression in EBV-immortalized latency III cells. Significantly, we show that overexpression of RGC-32 in B cells is sufficient to disrupt G2 cell-cycle arrest consistent with activation of CDK1, implicating RGC-32 in the EBV transformation process. Surprisingly, RGC-32 mRNA is expressed at high levels in latency I Burkitt's lymphoma (BL) cells and in some EBV-negative BL cell-lines, although RGC-32 protein expression is not detectable. We show that RGC-32 mRNA expression is elevated in latency I cells due to transcriptional activation by high levels of the differentially expressed RUNX1c transcription factor. We found that proteosomal degradation or blocked cytoplasmic export of the RGC-32 message were not responsible for the lack of RGC-32 protein expression in latency I cells. Significantly, analysis of the ribosomal association of the RGC-32 mRNA in latency I and latency III cells revealed that RGC-32 transcripts were associated with multiple ribosomes in both cell-types implicating post-initiation translational repression mechanisms in the block to RGC-32 protein production in latency I cells. In summary, our results are the first to demonstrate RGC-32 protein upregulation in cells transformed by a human tumour virus and to identify post-initiation translational mechanisms as an expression control point for this key cell-cycle regulator

Post-Stenotic Recirculating Flow May Cause Hemodynamic Perforator Infarction

Background and Purpose The primary mechanism underlying paramedian pontine infarction (PPI) is atheroma obliterating the perforators. Here, we encountered a patient with PPI in the post-stenotic area of basilar artery (BA) without a plaque, shown, by high-resolution magnetic resonance imaging (HR-MRI). We performed an experiment using a 3D-printed BA model and a particle image velocimetry (PIV) to explore the hemodynamic property of the post-stenotic area and the mechanism of PPI. Methods 3D-model of a BA stenosis was reconstructed with silicone compound using a 3D printer based on the source image of HR-MRI. Working fluid seeded with fluorescence particles was used and the velocity of those particles was measured horizontally and vertically. Furthermore, microtubules were inserted into the posterior aspect of the model to measure the flow rates of perforators (pre- and post-stenotic areas). The flow rates were compared between the microtubules. Results A recirculating flow was observed from the post-stenotic area in both directions forming a spiral shape. The velocity of the flow in these regions of recirculation was about one-tenth that of the flow in other regions. The location of recirculating flow well corresponded with the area with low-signal intensity at the time-of-flight magnetic resonance angiography and the location of PPI. Finally, the flow rate through the microtubule inserted into the post-stenotic area was significantly decreased comparing to others (P<0.001). Conclusions Perforator infarction may be caused by a hemodynamic mechanism altered by stenosis that induces a recirculation flow. 3D-printed modeling and PIV are helpful understanding the hemodynamics of intracranial stenosis.114Ysciescopu