Electrical Control of Magnetization in Charge-ordered Multiferroic LuFe2O4

LuFe2O4 exhibits multiferroicity due to charge order on a frustrated triangular lattice. We find that the magnetization of LuFe2O4 in the multiferroic state can be electrically controlled by applying voltage pulses. Depending on with or without magnetic fields, the magnetization can be electrically switched up or down. We have excluded thermal heating effect and attributed this electrical control of magnetization to an intrinsic magnetoelectric coupling in response to the electrical breakdown of charge ordering. Our findings open up a new route toward electrical control of magnetization.Comment: 14 pages, 5 figure

Image Data Compensation to Prevent Display Artifacts on an OLED Display

This publication describes techniques for image data compensation that prevent display artifacts on an organic light-emitting diode (OLED) display when the refresh rate and the clock speed of the display are changed. The OLED display may be implemented in a mobile device that supports multiple refresh rates. To conserve power, the mobile device may alter the refresh rate and clock speed of the OLED display from a first refresh rate and clock speed to a second refresh rate and clock speed. Image data intended to be displayed on a particular pixel row of the OLED display may be compensated based on the first refresh rate, the second refresh rate, and the location of the particular pixel row within the OLED display to generate compensated image data. Using the techniques described herein, the compensated image data may be output for use in preventing display artifacts while the image data is displayed in a first frame after the refresh rate and clock speed are changed

Limits of Binaries That Can Be Characterized by Gravitational Microlensing

Due to the high efficiency of planet detections, current microlensing planet searches focus on high-magnification events. High-magnification events are sensitive to remote binary companions as well and thus a sample of wide-separation binaries are expected to be collected as a byproduct. In this paper, we show that characterizing binaries for a portion of this sample will be difficult due to the degeneracy of the binary-lensing parameters. This degeneracy arises because the perturbation induced by the binary companion is well approximated by the Chang-Refsdal lensing for binaries with separations greater than a certain limit. For binaries composed of equal mass lenses, we find that the lens binarity can be noticed up to the separations of $\sim 60$ times of the Einstein radius corresponding to the mass of each lens. Among these binaries, however, we find that the lensing parameters can be determined only for a portion of binaries with separations less than $\sim 20$ times of the Einstein radius.Comment: 5 pages, 3 figures, 1 tabl

S100a9 Knockdown Decreases the Memory Impairment and the Neuropathology in Tg2576 Mice, AD Animal Model

Inflammation, insoluble protein deposition and neuronal cell loss are important features in the Alzheimer's disease (AD) brain. To investigate the regulatory genes responsible for the neuropathology in AD, we performed microarray analysis with APPV717I-CT100 transgenic mice, an animal model of AD, and isolated the S100a9 gene, which encodes an inflammation-associated calcium binding protein. In another AD animal model, Tg2576 mouse brain, and in human AD brain, induction of S100a9 was confirmed. The endogenous expression of S100a9 was induced by treatment with Aβ or CT peptides in a microglia cell line, BV2 cells. In these cells, silencing study of S100a9 showed that the induction of S100a9 increased the intracellular calcium level and up-regulated the inflammatory cytokines (IL-1β and TNFα) and iNOS. S100a9 lentiviral short hairpin RNA (sh-S100a9) was injected into the hippocampus region of the brains of 13-month-old Tg2576 mice. At two months after injection, we found that knockdown of S100a9 expression had improved the cognition decline of Tg2576 mice in the water maze task, and had reduced amyloid plaque burden. These results suggest that S100a9 induced by Aβ or CT contributes to cause inflammation, which then affects the neuropathology including amyloid plaques burden and impairs cognitive function. Thus, the inhibition of S100a9 is a possible target for AD therapy