Faraday Rotation Measure due to the Intergalactic Magnetic Field

Studying the nature and origin of the intergalactic magnetic field (IGMF) is an outstanding problem of cosmology. Measuring Faraday rotation would be a promising method to explore the IGMF in the large-scale structure (LSS) of the universe. We investigated the Faraday rotation measure (RM) due to the IGMF in filaments of galaxies using simulations for cosmological structure formation. We employed a model IGMF based on turbulence dynamo in the LSS of the universe; it has an average strength of $\sim 10$ nG and a coherence length of several $\times\ 100\ h^{-1}$ kpc in filaments. With the coherence length smaller than path length, the inducement of RM would be a random walk process, and we found that the resultant RM is dominantly contributed by the density peak along line of sight. The rms of RM through filaments at the present universe was predicted to be $\sim 1\ {\rm rad\ m^{-2}}$. In addition, we predicted that the probability distribution function of $|{\rm RM}|$ through filaments follows the log-normal distribution, and the power spectrum of RM in the local universe peaks at a scale of $\sim 1\ h^{-1}$ Mpc. Our prediction of RM could be tested with future instruments.Comment: To appear in ApJ. Pdf with full resolution figures can be downloaded from http://canopus.cnu.ac.kr/ryu/ar.pd

Comparisons of Cosmological MHD Galaxy Cluster Simulations to Radio Observations

Radio observations of galaxy clusters show that there are $\mu$G magnetic fields permeating the intra-cluster medium (ICM), but it is hard to accurately constrain the strength and structure of the magnetic fields without the help of advanced computer simulations. We present qualitative comparisons of synthetic VLA observations of simulated galaxy clusters to radio observations of Faraday Rotation Measure (RM) and radio halos. The cluster formation is modeled using adaptive mesh refinement (AMR) magneto-hydrodynamic (MHD) simulations with the assumption that the initial magnetic fields are injected into the ICM by active galactic nuclei (AGNs) at high redshift. In addition to simulated clusters in Xu et al. (2010, 2011), we present a new simulation with magnetic field injections from multiple AGNs. We find that the cluster with multiple injection sources is magnetized to a similar level as in previous simulations with a single AGN. The RM profiles from simulated clusters, both $|RM|$ and the dispersion of RM ($\sigma_{RM}$), are consistent at a first-order with the radial distribution from observations. The correlations between the $\sigma_{RM}$ and X-ray surface brightness from simulations are in a broad agreement with the observations, although there is an indication that the simulated clusters could be slightly over-dense and less magnetized with respect to those in the observed sample. In addition, the simulated radio halos agree with the observed correlations between the radio power versus the cluster X-ray luminosity and between the radio power versus the radio halo size. These studies show that the cluster wide magnetic fields that originate from AGNs and are then amplified by the ICM turbulence (Xu et al. 2010) match observations of magnetic fields in galaxy clusters.Comment: Accepted for publication in Ap

Mutual Regulation Between Polo-like Kinase 3 and SIAH2 E3 Ubiquitin Ligase Defines a Regulatory Network That Fine-tunes the Cellular Response to Hypoxia and Nickel

Elevated cellular response to hypoxia, which contributes to cell transformation and tumor progression, is a prominent feature of malignant cells in solid tumors. Polo-like kinase 3 (Plk3) is a serine/threonine protein kinase known to inhibit the cellular response to hypoxia and tumorigenesis. Nickel compounds are well-established human carcinogens that induce tumorigenesis partly through their hypoxia-mimicking effects. Despite previous research efforts, the role of Plk3 in the hypoxic response induced by hypoxia or nickel is not completely understood. Here, we show that NiC

Gene 33/Mig6 Inhibits Hexavalent Chromium-Induced DNA Damage and Cell Transformation in Human Lung Epithelial Cells

Hexavalent Chromium [Cr(VI)] compounds are human lung carcinogens and environmental/occupational hazards. The molecular mechanisms of Cr(VI) carcinogenesis appear to be complex and are poorly defined. In this study, we investigated the potential role of Gene 33 (ERRFI1, Mig6), a multifunctional adaptor protein, in Cr(VI)-mediated lung carcinogenesis. We show that the level of Gene 33 protein is suppressed by both acute and chronic Cr(VI) treatments in a dose- and time-dependent fashion in BEAS-2B lung epithelial cells. The inhibition also occurs in A549 lung bronchial carcinoma cells. Cr(VI) suppresses Gene 33 expression mainly through post-transcriptional mechanisms, although the mRNA level of gene 33 also tends to be lower upon Cr(VI) treatments. Cr(VI)-induced DNA damage appears primarily in the S phases of the cell cycle despite the high basal DNA damage signals at the G2M phase. Knockdown of Gene 33 with siRNA significantly elevates Cr(VI)-induced DNA damage in both BEAS-2B and A549 cells. Depletion of Gene 33 also promotes Cr(VI)-induced micronucleus (MN) formation and cell transformation in BEAS-2B cells. Our results reveal a novel function of Gene 33 in Cr(VI)-induced DNA damage and lung epithelial cell transformation. We propose that in addition to its role in the canonical EGFR signaling pathway and other signaling pathways, Gene 33 may also inhibit Cr(VI)-induced lung carcinogenesis by reducing DNA damage triggered by Cr(VI)