Self-induced charge currents in electromagnetic materials, photon effective rest mass and some related topics

The contribution of self-induced charge currents of metamaterial media to photon effective rest mass is discussed in detail in the present paper. We concern ourselves with two kinds of photon effective rest mass, i.e., the frequency-dependent and frequency-independent effective rest mass. Based on these two definitions, we calculate the photon effective rest mass in the left-handed medium and the 2TDLM media, the latter of which is described by the so-called two time derivative Lorentz material (2TDLM) model. Additionally, we concentrate primarily on the torque, which is caused by the interaction between self-induced charge currents in dilute plasma (e.g., the secondary cosmic rays) and interstellar magnetic fields (ambient cosmic magnetic vector potentials), acting on the torsion balance of the rotating torsion balance experiment.Comment: 11 pages, Late

Reconfigurable quantum metamaterials

By coupling controllable quantum systems into larger structures we introduce the concept of a quantum metamaterial. Conventional meta-materials represent one of the most important frontiers in optical design, with applications in diverse fields ranging from medicine to aerospace. Up until now however, metamaterials have themselves been classical structures and interact only with the classical properties of light. Here we describe a class of dynamic metamaterials, based on the quantum properties of coupled atom-cavity arrays, which are intrinsically lossless, reconfigurable, and operate fundamentally at the quantum level. We show how this new class of metamaterial could be used to create a reconfigurable quantum superlens possessing a negative index gradient for single photon imaging. With the inherent features of quantum superposition and entanglement of metamaterial properties, this new class of dynamic quantum metamaterial, opens a new vista for quantum science and technology.Comment: 16 pages, 8 figure

Preparation and control of a cavity-field state through atom-driven field interaction: towards long-lived mesoscopic states

The preparation of mesoscopic states of the radiation and matter fields through atom-field interactions has been achieved in recent years and employed for a range of striking applications in quantum optics. Here we present a technique for the preparation and control of a cavity mode which, besides interacting with a two-level atom, is simultaneously submitted to linear and parametric amplification processes. The role of the amplification-controlling fields in the achievement of real mesoscopic states, is to produce highly-squeezed field states and, consequently, to increase both: i) the distance in phase space between the components of the prepared superpositions and ii) the mean photon number of such superpositions. When submitting the squeezed superposition states to the action of similarly squeezed reservoirs, we demonstrate that under specific conditions the decoherence time of the states becomes independent of both the distance in phase space between their components and their mean photon number. An explanation is presented to support this remarkable result, together with a discussion on the experimental implementation of our proposal. We also show how to produce number states with fidelities higher than those derived as circular states

Nitric oxide differentially regulates renal ATP-binding cassette transporters during endotoxemia

Nitric oxide (NO) is an important regulator of renal transport processes. In the present study, we investigated the role of NO, produced by inducible NO synthase (iNOS), in the regulation of renal ATP-binding cassette (ABC) transporters in vivo during endotoxemia. Wistar–Hannover rats were injected with lipopolysaccharide (LPS+) alone or in combination with the iNOS inhibitor, aminoguanidine. Controls received detoxified LPS (LPS−). After LPS+, proximal tubular damage and a reduction in renal function were observed. Furthermore, iNOS mRNA and protein, and the amount of NO metabolites in plasma and urine, increased compared to the LPS− group. Coadministration with aminoguanidine resulted in an attenuation of iNOS induction and reduction of renal damage. Gene expression of 20 ABC transporters was determined. After LPS+, a clear up-regulation in Abca1, Abcb1/P-glycoprotein (P-gp), Abcb11/bile salt export pump (Bsep), and Abcc2/multidrug resistance protein (Mrp2) was found, whereas Abcc8 was down-regulated. Up-regulation of Abcc2/Mrp2 was accompanied by enhanced calcein excretion. Aminoguanidine attenuated the effects on transporter expression. Our data indicate that NO, produced locally by renal iNOS, regulates the expression of ABC transporters in vivo. Furthermore, we showed, for the first time, expression and subcellular localization of Abcb11/Bsep in rat kidney

Kaposi's Sarcoma Associated Herpes Virus (KSHV) Induced COX-2: A Key Factor in Latency, Inflammation, Angiogenesis, Cell Survival and Invasion

Kaposi's sarcoma (KS), an enigmatic endothelial cell vascular neoplasm, is characterized by the proliferation of spindle shaped endothelial cells, inflammatory cytokines (ICs), growth factors (GFs) and angiogenic factors. KSHV is etiologically linked to KS and expresses its latent genes in KS lesion endothelial cells. Primary infection of human micro vascular endothelial cells (HMVEC-d) results in the establishment of latent infection and reprogramming of host genes, and cyclooxygenase-2 (COX-2) is one of the highly up-regulated genes. Our previous study suggested a role for COX-2 in the establishment and maintenance of KSHV latency. Here, we examined the role of COX-2 in the induction of ICs, GFs, angiogenesis and invasive events occurring during KSHV de novo infection of endothelial cells. A significant amount of COX-2 was detected in KS tissue sections. Telomerase-immortalized human umbilical vein endothelial cells supporting KSHV stable latency (TIVE-LTC) expressed elevated levels of functional COX-2 and microsomal PGE2 synthase (m-PGES), and secreted the predominant eicosanoid inflammatory metabolite PGE2. Infected HMVEC-d and TIVE-LTC cells secreted a variety of ICs, GFs, angiogenic factors and matrix metalloproteinases (MMPs), which were significantly abrogated by COX-2 inhibition either by chemical inhibitors or by siRNA. The ability of these factors to induce tube formation of uninfected endothelial cells was also inhibited. PGE2, secreted early during KSHV infection, profoundly increased the adhesion of uninfected endothelial cells to fibronectin by activating the small G protein Rac1. COX-2 inhibition considerably reduced KSHV latent ORF73 gene expression and survival of TIVE-LTC cells. Collectively, these studies underscore the pivotal role of KSHV induced COX-2/PGE2 in creating KS lesion like microenvironment during de novo infection. Since COX-2 plays multiple roles in KSHV latent gene expression, which themselves are powerful mediators of cytokine induction, anti-apoptosis, cell survival and viral genome maintainence, effective inhibition of COX-2 via well-characterized clinically approved COX-2 inhibitors could potentially be used in treatment to control latent KSHV infection and ameliorate KS

Uracil DNA N-Glycosylase Promotes Assembly of Human Centromere Protein A

Uracil is removed from DNA by the conserved enzyme Uracil DNA N-glycosylase (UNG). Previously, we observed that inhibiting UNG in Xenopus egg extracts blocked assembly of CENP-A, a histone H3 variant. CENP-A is an essential protein in all species, since it is required for chromosome segregation during mitosis. Thus, the implication of UNG in CENP-A assembly implies that UNG would also be essential, but UNG mutants lacking catalytic activity are viable in all species. In this paper, we present evidence that UNG2 colocalizes with CENP-A and H2AX phosphorylation at centromeres in normally cycling cells. Reduction of UNG2 in human cells blocks CENP-A assembly, and results in reduced cell proliferation, associated with increased frequencies of mitotic abnormalities and rapid cell death. Overexpression of UNG2 induces high levels of CENP-A assembly in human cells. Using a multiphoton laser approach, we demonstrate that UNG2 is rapidly recruited to sites of DNA damage. Taken together, our data are consistent with a model in which the N-terminus of UNG2 interacts with the active site of the enzyme and with chromatin