Asymmetric-valued Spectrum Auction and Competition in Wireless Broadband Services

We study bidding and pricing competition between two spiteful mobile network operators (MNOs) with considering their existing spectrum holdings. Given asymmetric-valued spectrum blocks are auctioned off to them via a first-price sealed-bid auction, we investigate the interactions between two spiteful MNOs and users as a three-stage dynamic game and characterize the dynamic game's equilibria. We show an asymmetric pricing structure and different market share between two spiteful MNOs. Perhaps counter-intuitively, our results show that the MNO who acquires the less-valued spectrum block always lowers his service price despite providing double-speed LTE service to users. We also show that the MNO who acquires the high-valued spectrum block, despite charing a higher price, still achieves more market share than the other MNO. We further show that the competition between two MNOs leads to some loss of their revenues. By investigating a cross-over point at which the MNOs' profits are switched, it serves as the benchmark of practical auction designs

サブ0.3V動作超低消費電力MOSFETのデバイス設計指針に関する研究

学位の種別: 課程博士審査委員会委員 : （主査）東京大学教授 平本 俊郎, 東京大学教授 桜井 貴康, 東京大学教授 高木 信一, 東京大学准教授 竹中 充, 東京大学准教授 喜多 浩之, 東京大学准教授 小林 正治University of Tokyo(東京大学

Hydrated copper and gold monovalent cations: Ab initio study

To understand the hydration phenomena of noble transition metals, we investigated the structures, hydration energies, electronic properties, and spectra of the Cu+(H3O)(1-6) and Au+ (H2O)(1-6) clusters using ab initio calculations. The coordination numbers of these clusters are found to be only two, which is highly contrasted to those of Ag+ (H2O)(n) (which have the coordination numbers of 3-4) as well as the hydrated alkali metal ions (which have the coordination numbers of similar to6). For the possible identification of their interesting hydration structures, we predict their IR spectra for the OH stretch modes. (C) 2005 American Institute of Physics.open384

De novo copy number variations in cloned dogs from the same nuclear donor

BACKGROUND: Somatic mosaicism of copy number variants (CNVs) in human body organs and de novo CNV event in monozygotic twins suggest that de novo CNVs can occur during mitotic recombination. These de novo CNV events are important for understanding genetic background of evolution and diverse phenotypes. In this study, we explored de novo CNV event in cloned dogs with identical genetic background. RESULTS: We analyzed CNVs in seven cloned dogs using the nuclear donor genome as reference by array-CGH, and identified five de novo CNVs in two of the seven clones. Genomic qPCR, dye-swap array-CGH analysis and B-allele profile analysis were used for their validation. Two larger de novo CNVs (5.2 Mb and 338 Kb) on chromosomes X and 19 in clone-3 were consistently validated by all three experiments. The other three smaller CNVs (sized from 36.1 to76.4 Kb) on chromosomes 2, 15 and 32 in clone-3 and clone-6 were verified by at least one of the three validations. In addition to the de novo CNVs, we identified a 37 Mb-sized copy neutral de novo loss of heterozygosity event on chromosome 2 in clone-6. CONCLUSIONS: To our knowledge, this is the first report of de novo CNVs in the cloned dogs which were generated by somatic cell nuclear transfer technology. To study de novo genetic events in cloned animals can help understand formation mechanisms of genetic variants and their biological implications

Identification of gp96 as a Novel Target for Treatment of Autoimmune Disease in Mice

Heat shock proteins have been implicated as endogenous activators for dendritic cells (DCs). Chronic expression of heat shock protein gp96 on cell surfaces induces significant DC activations and systemic lupus erythematosus (SLE)-like phenotypes in mice. However, its potential as a therapeutic target against SLE remains to be evaluated. In this work, we conducted chemical approach to determine whether SLE-like phenotypes can be compromised by controlling surface translocation of gp96. From screening of chemical library, we identified a compound that binds and suppresses surface presentation of gp96 by facilitating its oligomerization and retrograde transport to endoplasmic reticulum. In vivo administration of this compound reduced maturation of DCs, populations of antigen presenting cells, and activated B and T cells. The chemical treatment also alleviated the SLE-associated symptoms such as glomerulonephritis, proteinuria, and accumulation of anti-nuclear and –DNA antibodies in the SLE model mice resulting from chronic surface exposure of gp96. These results suggest that surface translocation of gp96 can be chemically controlled and gp96 as a potential therapeutic target to treat autoimmune disease like SLE