A method of measuring the amplitude-modulated vacuum field near a conducting mirror

Electromagnetic fields of the vacuum mode near a conducting mirror are modified with respect to those in free space, with their amplitudes having a sinusoidal spatial dependence from the mirror. Therefore if we combine this spatially amplitude-modulated vacuum field mode and intense coherent light with a beam splitter, we may detect this fluctuation of the vacuum mode in a homodyne detection scheme. It will give a new method to produce squeezed states of light with a single mirror placed close to an unused port of a beam splitter. We show that the amplitude fluctuation of the combined light can be reduced by a factor of 2 below that of the coherent light. We also discuss the limitations due to the finite line width of the laser and the effective absorption length of the photodiodes

Transcriptional Regulator TonEBP Mediates Oxidative Damages in Ischemic Kidney Injury

TonEBP (tonicity-responsive enhancer binding protein) is a transcriptional regulator whose expression is elevated in response to various forms of stress including hyperglycemia, inflammation, and hypoxia. Here we investigated the role of TonEBP in acute kidney injury (AKI) using a line of TonEBP haplo-deficient mice subjected to bilateral renal ischemia followed by reperfusion (I/R). In the TonEBP haplo-deficient animals, induction of TonEBP, oxidative stress, inflammation, cell death, and functional injury in the kidney in response to I/R were all reduced. Analyses of renal transcriptome revealed that genes in several cellular pathways including peroxisome and mitochondrial inner membrane were suppressed in response to I/R, and the suppression was relieved in the TonEBP deficiency. Production of reactive oxygen species (ROS) and the cellular injury was reproduced in a renal epithelial cell line in response to hypoxia, ATP depletion, or hydrogen peroxide. The knockdown of TonEBP reduced ROS production and cellular injury in correlation with increased expression of the suppressed genes. The cellular injury was also blocked by inhibitors of necrosis. These results demonstrate that ischemic insult suppresses many genes involved in cellular metabolism leading to local oxidative stress by way of TonEBP induction. Thus, TonEBP is a promising target to prevent AKI