Anomalous low temperature state of CeOs4Sb12: Magnetic field and La-impurity study

Specific heat for single crystalline samples of Ce1-xLaxOs4Sb12 at zero-field and magnetic fields to 14 T is reported. Our results confirm enhanced value of the electronic specific heat coefficient in the paramagnetic state. They provide arguments for the intrinsic origin of the 1.1 K anomaly. This transition leads to opening of the gap at the Fermi surface. This low temperature state of CeOs4Sb12 is extremely sensitive to chemical impurities. 2% of La substituted for Ce suppresses the transition and reduces the electronic specific heat coefficient. The magnetic field response of the specific heat is also anomalous.Comment: 4 pages, 3 figure

Simulation of Arc Motion in Alternating Mahnetic Field Using Dimensionless Momentum Equation

A new heat-treatment system has been developed using an arc driven by an alternating magnetic field. The arc motion was theoretically investigated by the method of non-dimensionalanalysis. After the definition of the pertinent characteristic length and time, the momentum equation was converted into the dimensionless form. This approach gave us not only a short cut to simulate the arc motion but also clear understanding on the nature of the magnetically driven arc

Statistical mechanical analysis of the linear vector channel in digital communication

A statistical mechanical framework to analyze linear vector channel models in digital wireless communication is proposed for a large system. The framework is a generalization of that proposed for code-division multiple-access systems in Europhys. Lett. 76 (2006) 1193 and enables the analysis of the system in which the elements of the channel transfer matrix are statistically correlated with each other. The significance of the proposed scheme is demonstrated by assessing the performance of an existing model of multi-input multi-output communication systems.Comment: 15 pages, 2 figure

Probing Ion-Ion and Electron-Ion Correlations in Liquid Metals within the Quantum Hypernetted Chain Approximation

We use the Quantum Hypernetted Chain Approximation (QHNC) to calculate the ion-ion and electron-ion correlations for liquid metallic Li, Be, Na, Mg, Al, K, Ca, and Ga. We discuss trends in electron-ion structure factors and radial distribution functions, and also calculate the free-atom and metallic-atom form-factors, focusing on how bonding effects affect the interpretation of X-ray scattering experiments, especially experimental measurements of the ion-ion structure factor in the liquid metallic phase.Comment: RevTeX, 19 pages, 7 figure

Micro(mi) RNA-34a targets protein phosphatase (PP)1γ to regulate DNA damage tolerance.

The DNA damage response (DDR) triggers widespread changes in gene expression, mediated partly by alterations in micro(mi) RNA levels, whose nature and significance remain uncertain. Here, we report that miR-34a, which is upregulated during the DDR, modulates the expression of protein phosphatase 1γ (PP1γ) to regulate cellular tolerance to DNA damage. Multiple bio-informatic algorithms predict that miR-34a targets the PP1CCC gene encoding PP1γ protein. Ionising radiation (IR) decreases cellular expression of PP1γ in a dose-dependent manner. An miR-34a-mimic reduces cellular PP1γ protein. Conversely, an miR-34a inhibitor antagonizes IR-induced decreases in PP1γ protein expression. A wild-type (but not mutant) miR-34a seed match sequence from the 3' untranslated region (UTR) of PP1CCC when transplanted to a luciferase reporter gene makes it responsive to an miR-34a-mimic. Thus, miR-34a upregulation during the DDR targets the 3' UTR of PP1CCC to decrease PP1γ protein expression. PP1γ is known to antagonize DDR signaling via the ataxia-telangiectasia-mutated (ATM) kinase. Interestingly, we find that cells exposed to DNA damage become more sensitive - in an miR-34a-dependent manner - to a second challenge with damage. Increased sensitivity to the second challenge is marked by enhanced phosphorylation of ATM and p53, increased γH2AX formation, and increased cell death. Increased sensitivity can be partly recapitulated by a miR-34a-mimic, or antagonized by an miR-34a-inhibitor. Thus, our findings suggest a model in which damage-induced miR-34a induction reduces PP1γ expression and enhances ATM signaling to decrease tolerance to repeated genotoxic challenges. This mechanism has implications for tumor suppression and the response of cancers to therapeutic radiation.Work in ARV's laboratory is funded by the Medical Research Council.This is the author accepted manuscript. The final version is available from Taylor & Francis via http://dx.doi.org/10.1080/15384101.2015.106420