Anomalous Hall effect in a two-dimensional electron gas

The anomalous Hall effect in a magnetic two-dimensional electron gas with Rashba spin-orbit coupling is studied within the Kubo-Streda formalism in the presence of pointlike potential impurities. We find that all contributions to the anomalous Hall conductivity vanish to leading order in disorder strength when both chiral subbands are occupied. In the situation that only the majority subband is occupied, all terms are finite in the weak scattering limit and the total anomalous Hall conductivity is dominated by skew scattering. We compare our results to previous treatments and resolve some of the discrepancies present in the literature.Comment: 11 pages, 5 figure

8GHz帯域における高温超電導フィルタの研究<平成12年度 共同研究の概要>

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Anomalous Hall effect in a two-dimensional electron gas

The anomalous Hall effect in a magnetic two-dimensional electron gas with Rashba spin-orbit coupling is studied within the Kubo-Streda formalism in the presence of pointlike potential impurities. We find that all contributions to the anomalous Hall conductivity vanish to leading order in disorder strength when both chiral subbands are occupied. In the situation that only the majority subband is occupied, all terms are finite in the weak scattering limit and the total anomalous Hall conductivity is dominated by skew scattering. We compare our results to previous treatments and resolve some of the discrepancies present in the literature.journal articl

Evidence for Muon Neutrino Oscillation in an Accelerator-Based Experiment

journal articl

シロイヌナズナ RKD4 イデンシ ニ ヨル ハイ ハッセイ セイギョ キコウ ノ カイセキ

奈良先端科学技術大学院大学博士(バイオサイエンス)doctoral thesi

Comparison of Experimental Data and Computer Simulations

<div><p>Data are shown for the three gene networks described in <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0030064#pbio-0030064-g003" target="_blank">Figure 3</a>, showing outputs for proteins A (cyan), B (magenta) and C (dark blue).</p> <p>(A) Quantitated Western blot data from <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0030064#pbio-0030064-g003" target="_blank">Figure 3</a>, after 25 min.</p> <p>(B) Simulation data plotted as percentage of total output protein against chamber length, at the chamber (18-mm) or <i>Drosophila</i> (0.5-mm) scale. The model is described in full in <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0030064#sd001" target="_blank">Protocol S1</a>.</p></div

Alternative Gene Networks

<div><p>At five set time points (15, 25, 35, 60, and 90 min), transcription-translation chambers were dissected into nine slabs for Western blot analysis.</p> <p>(A) Control network with no repression sites between genes A, B, and C.</p> <p>(B) Minimally repressed network (compare <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0030064#pbio-0030064-g001" target="_blank">Figure 1</a>).</p> <p>(C) Mutual repression network with extensive negative interactions between species. Adding protease (“+ Degradation”) creates weak but time-stable patterns for both the “Repressed” and “Mutual” networks (35 versus 90 min). Quantitated graphs for the above data are available in <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0030064#sd001" target="_blank">Protocol S1</a>.</p></div

Gene Circuits and Chambers

<div><p>(A) Principal interactions in the <i>Drosophila</i> gap gene network, modelled after [<a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.0030064#pbio-0030064-b37" target="_blank">37</a>]. Relative levels and distributions of Hunchback (Hb), Giant (Gt), Krüppel (Kr), Knirps (Kni), Bicoid (Bcd), and Caudal (Cad) shown from anterior (left) to posterior (right). Green arrows indicate activation, red T-bars repression.</p> <p>(B) Artificial gene network design, with transcription activators T7 and SP6 polymerases, and zinc finger repressors A, B, and C. Genes are immobilised on paramagnetic beads, and T7 forms a directional concentration gradient.</p> <p>(C) Principal interactions in a simple designed network.</p> <p>(D) Transcription-translation chamber. Genes for repressor A are localised at the “poles,” whereas B and C are ubiquitous. Gel slabs 4–6 have been excised, exposing the magnets below, illustrating gel dissection for Western blot analysis.</p> <p>(E) Normalised Western data for four replicate chambers, showing mean levels of A, B, and C after 20 min (± One standard deviation).</p> <p>(F) Sample Western blot from the four-replicate experiment.</p></div

Engineering Gene Networks to Emulate <em>Drosophila</em> Embryonic Pattern Formation

<div><p>Pattern formation is essential in the development of higher eukaryotes. For example, in the <em>Drosophila</em> embryo, maternal morphogen gradients establish gap gene expression domain patterning along the anterior-posterior axis, through linkage with an elaborate gene network. To understand the evolution and behaviour of such systems better, it is important to establish the minimal determinants required for patterning. We have therefore engineered artificial transcription-translation networks that generate simple patterns, crudely analogous to the <em>Drosophila</em> gap gene system. The <em>Drosophila</em> syncytium was modelled using DNA-coated paramagnetic beads fixed by magnets in an artificial chamber, forming a gene expression network. Transient expression domain patterns were generated using various levels of network connectivity. Generally, adding more transcription repression interactions increased the “sharpness” of the pattern while reducing overall expression levels. An accompanying computer model for our system allowed us to search for parameter sets compatible with patterning. While it is clear that the <em>Drosophila</em> embryo is far more complex than our simplified model, several features of interest emerge. For example, the model suggests that simple diffusion may be too rapid for <em>Drosophila</em>-scale patterning, implying that sublocalisation, or “trapping,” is required. Second, we find that for pattern formation to occur under the conditions of our in vitro reaction-diffusion system, the activator molecules must propagate faster than the inhibitors. Third, adding controlled protease degradation to the system stabilizes pattern formation over time. We have reconstituted transcriptional pattern formation from purified substances, including phage RNA polymerases, ribonucleotides, and an eukaryotic translation extract. We anticipate that the system described here will be generally applicable to the study of any biological network with a spatial component.</p> </div

Map of the Constructs Used in This Study

<p>The repressor binding sites overlap with T7 or SP6 promoters and vary between constructs. In this way, it is possible to alter the connectivity of the repressive interactions by the products of genes A, B, and C. Repressive interactions are denoted by T-bars. The start codon of each gene is in Kozak context and is denoted by “GCC ATG G.”</p