Anomalous Anisotropic Magnetoresistance in Heavy-Fermion PrFe4P12

We have investigated the anisotropy of the magnetoresistance in the Pr-based HF compound PrFe4P12. The large anisotropy of effective mass and its strong field dependence have been confirmed by resistivity measurements. Particularly for H||[111], where the effective mass is most strongly enhanced, the non-Fermi liquid behavior has been observed. Also, we have found the angular dependence of the magnetoresistance sharply enhanced at H||[111], which is evidently correlated with both the non-Fermi liquid behavior and the high-field ordered state (B-phase).Comment: 3 pages, 3 figures. J. Phys. Soc. Jpn. Vol.77, No.8, in pres

On the origin of multiple ordered phases in PrFe4P12

The nature of multiple electronic orders in skutterudite PrFe_4P_{12} is discussed on the basis of a model with antiferro-quadrupole (AFQ) interaction of \Gamma_3 symmetry. The high-field phase can be reproduced qualitatively provided (i) ferro-type interactions are introduced between the dipoles as well as between the octupoles of localized f-electrons, and (ii) separation is vanishingly small between the \Gamma_1-\Gamma_4^{(1)} crystalline electric field (CEF) levels. The high-field phase can have either the same ordering vector q=(1,0,0) as in the low-field phase, or a different one q=0 depending on the parameters. In the latter case, distortion of the crystal perpendicular to the (111) axis is predicted. The corresponding anomaly in elastic constants should also appear. The electrical resistivity is calculated with account of scattering within the CEF quasi-quartet. It is found that the resistivity as a function of the direction of magnetic field shows a sharp maximum around the (111) axis at low temperatures because of the level crossing.Comment: 16 pages, 5 figure

Fast Purcell-enhanced single photon source in 1,550-nm telecom band from a resonant quantum dot-cavity coupling

High-bit-rate nanocavity-based single photon sources in the 1,550-nm telecom band are challenges facing the development of fibre-based long-haul quantum communication networks. Here we report a very fast single photon source in the 1,550-nm telecom band, which is achieved by a large Purcell enhancement that results from the coupling of a single InAs quantum dot and an InP photonic crystal nanocavity. At a resonance, the spontaneous emission rate was enhanced by a factor of 5 resulting a record fast emission lifetime of 0.2 ns at 1,550 nm. We also demonstrate that this emission exhibits an enhanced anti-bunching dip. This is the first realization of nanocavity-enhanced single photon emitters in the 1,550-nm telecom band. This coupled quantum dot cavity system in the telecom band thus provides a bright high-bit-rate non-classical single photon source that offers appealing novel opportunities for the development of a long-haul quantum telecommunication system via optical fibres.Comment: 16 pages, 4 figure

Defending the genome from the enemy within:mechanisms of retrotransposon suppression in the mouse germline

The viability of any species requires that the genome is kept stable as it is transmitted from generation to generation by the germ cells. One of the challenges to transgenerational genome stability is the potential mutagenic activity of transposable genetic elements, particularly retrotransposons. There are many different types of retrotransposon in mammalian genomes, and these target different points in germline development to amplify and integrate into new genomic locations. Germ cells, and their pluripotent developmental precursors, have evolved a variety of genome defence mechanisms that suppress retrotransposon activity and maintain genome stability across the generations. Here, we review recent advances in understanding how retrotransposon activity is suppressed in the mammalian germline, how genes involved in germline genome defence mechanisms are regulated, and the consequences of mutating these genome defence genes for the developing germline

Cyclosporin A Associated Helicase-Like Protein Facilitates the Association of Hepatitis C Virus RNA Polymerase with Its Cellular Cyclophilin B

BACKGROUND: Cyclosporin A (CsA) is well known as an immunosuppressive drug useful for allogeneic transplantation. It has been reported that CsA inhibits hepatitis C virus (HCV) genome replication, which indicates that cellular targets of CsA regulate the viral replication. However, the regulation mechanisms of HCV replication governed by CsA target proteins have not been fully understood. PRINCIPAL FINDINGS: Here we show a chemical biology approach that elucidates a novel mechanism of HCV replication. We developed a phage display screening to investigate compound-peptide interaction and identified a novel cellular target molecule of CsA. This protein, named CsA associated helicase-like protein (CAHL), possessed RNA-dependent ATPase activity that was negated by treatment with CsA. The downregulation of CAHL in the cells resulted in a decrease of HCV genome replication. CAHL formed a complex with HCV-derived RNA polymerase NS5B and host-derived cyclophilin B (CyPB), known as a cellular cofactor for HCV replication, to regulate NS5B-CyPB interaction. CONCLUSIONS: We found a cellular factor, CAHL, as CsA associated helicase-like protein, which would form trimer complex with CyPB and NS5B of HCV. The strategy using a chemical compound and identifying its target molecule by our phage display analysis is useful to reveal a novel mechanism underlying cellular and viral physiology

Computational genes: a tool for molecular diagnosis and therapy of aberrant mutational phenotype

<p>Abstract</p> <p>Background</p> <p>A finite state machine manipulating information-carrying DNA strands can be used to perform autonomous molecular-scale computations at the cellular level.</p> <p>Results</p> <p>We propose a new finite state machine able to detect and correct aberrant molecular phenotype given by mutated genetic transcripts. The aberrant mutations trigger a cascade reaction: specific molecular markers as input are released and induce a spontaneous self-assembly of a wild type protein or peptide, while the mutational disease phenotype is silenced. We experimentally demostrated in <it>in vitro </it>translation system that a viable protein can be autonomously assembled.</p> <p>Conclusion</p> <p>Our work demostrates the basic principles of computational genes and particularly, their potential to detect mutations, and as a response thereafter administer an output that suppresses the aberrant disease phenotype and/or restores the lost physiological function.</p