Fine Features in the Primordial Power Spectrum

A possible origin of the anomalous dip and bump in the primordial power spectrum, which are reconstructed from WMAP data corresponding to the multipole $\ell=100\sim 140$ by using the inversion method, is investigated as a consequence of modification of scalar field dynamics in the inflation era. Utilizing an analytic formula to handle higher order corrections to the slow-roll approximation, we evaluate the relation between a detailed shape of inflaton potential and a fine structure in the primordial power spectrum. We conclude that it is unlikely to generate the observed dip and bump in the power spectrum by adding any features in the inflaton potential. Though we can make a fine enough shape in the power spectrum by controlling the feature of the potential, the amplitude of the dip and bump becomes too small in that case.Comment: 15 pages, 11 figures, submitted to JCA

Exploring the intergalactic magnetic field by means of Faraday tomography

Unveiling the intergalactic magnetic field (IGMF) in filaments of galaxies is a very important and challenging subject in modern astronomy. In order to probe the IGMF from rotation measures (RMs) of extragalactic radio sources, we need to separate RMs due to other origins such as the source, intervening galaxies, and our Galaxy. In this paper, we discuss observational strategies for the separation by means of Faraday tomography (Faraday RM synthesis). We consider an observation of a single radio source such as a radio galaxy or a quasar viewed through the Galaxy and the cosmic web. We then compare the observation with another observation of a neighboring source with a small angular separation. Our simulations with simple models of the sources suggest that it would be not easy to detect the RM due to an IGMF of order ??? 1 rad m-2, an expected value for the IGMF through a single filament. Contrary to this, we find that an RM of at least ??? 10 rad m-2 could be detected with the Square Kilometre Array or its pathfinders/precursors, if we achieve selection of ideal sources. These results would be improved if we incorporated decomposition techniques such as RMCLEAN and QU-fitting. We discuss the feasibility of the strategies for cases with complex Galactic emissions as well as with effects of observational noise and radio frequency interferences.close2

Fisher analysis on wide-band polarimetry for probing the intergalactic magnetic field

We investigate the capability of current radio telescopes for probing Faraday rotation measure (RM) due to the intergalactic magnetic field (IGMF) in the large-scale structure of the universe, which is expected to be of order O (1) rad m-2. We consider polarization observations of a compact radio source such as quasars behind a diffuse source such as the Galaxy, and calculate Stokes parameters Q and U assuming a simple model of the Faraday dispersion functions with Gaussian shape. Then, we perform the Fisher analysis to estimate the expected errors in the model parameters from QU-fitting of polarization intensity, accounting for the sensitivities and frequency bands of Australian Square Kilometer Array Pathfinder, Low Frequency Array, and the Giant Meterwave Radio Telescope. Finally, we examine the conditions on the source intensities which are required to detect the IGMF. Our analysis indicates that the QU-fitting is promising for forthcoming wideband polarimetry to explore RM due to the IGMF in filaments of galaxies.close5

Extracellular Disposal of Tumor-Suppressor miRs-145 and -34a via Microvesicles and 5-FU Resistance of Human Colon Cancer Cells

The dysregulation of microRNA (miRNA) expression causes various kinds of diseases. Especially, alterations in miRNA expression levels are frequently observed in human tumor cells and are associated with cancer pathogenesis. Earlier we established Fluorouracil (5-FU)-resistant human colon cancer DLD-1 cells (DLD-1/5FU) from parental 5-FU- sensitive DLD-1 cells. In the present study, we examined the expression of miRNA in each cell line and in its extracellular microvesicles (MVs) before and after treatment with 5-FU. The nascent RNAs of anti-oncogenic miR-34a and -145 labeled with EU in both cells were proved to be transferred into MVs in both cell lines. The levels of miR-34a and -145 in the cells and in their MVs were not largely different in the two cell lines, and a substantial amount of both miRNAs was secreted by both cell lines even in the steady-state condition. The exposure of both cell lines to 5-FU significantly increased the intracellular levels of miR-145 and miR-34a in the 5-FU-sensitive DLD-1 cells, whereas the level of neither miR was elevated in the DLD-1/5FU cells. Interestingly, the amount of miR-145 detected in the small MVs shed into the medium of the parental cells was reduced after the treatment with 5-FU. On the other hand, the intracellular expression of miR-34a in the DLD-1/5FU cells was down-regulated compared with that in the parental DLD-1 cells even in the steady-state condition. As to the miR-34a secreted into MVs, the increase in the level in DLD-1/5FU cells was greater than that in the parental DLD-1 cells after the treatment with 5-FU. Thus, the intra- and extracellular miR-145 and -34a were closely associated with 5-FU resistance, and the resistance was in part due to the enhanced secretion of miR-145 and -34a via MVs, resulting in low intracellular levels of both miRNAs

A Novel Role of Dickkopf-Related Protein 3 in Macropinocytosis in Human Bladder Cancer T24 Cells

Dickkopf-related protein 3 (Dkk-3) is a potential tumor suppressor reported in various cancer entities. However, we found that Dkk-3 was exceptionally upregulated in bladder cancer T24 cells. To validate the biological role of Dkk-3 other than a tumor suppressor, we examined the function of Dkk-3 in T24 cells. Gene silencing of Dkk-3 inhibited cell growth through inducing G0/G1 cell-cycle arrest. Furthermore, Dkk-3 knock-down caused macropinocytosis accompanied by autophagy, which were canceled in part by their inhibitors 5-(N-ethyl-N-isopropyl) amiloride (EIPA) and 3-methyladenine (3-MA). The macropinocytosis was induced by the Dkk-3 knock-down when there were sufficient extracellular nutrients. On the other hand, when the nutritional condition was poor, the autophagy was mainly induced by the Dkk-3 knock-down. These data indicated that Dkk-3 has a role in modulating macropinocytotic and autophagic pathways, a distinct function other than a Wnt antagonist