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Kalai-Smorodinsky Bargaining Solution and Alternating Offers Game  [PDF]
Yoichi Nishihara
Theoretical Economics Letters (TEL) , 2013, DOI: 10.4236/tel.2013.31012
Abstract: This article presents an alternating offers game that supports a Kalai-Smorodinsky bargaining solution (KSS). It is well known that a solution to an alternating offers game has a breakdown point equivalent to a status quo that converges to its Nash bargaining solution because the probability of breakdown becomes negligible, whereas we show that a KSS is obtained if a breakdown gives everything to the player who rejects. The former option, which is adopted by many application papers may be suitable for ex ante production. However, the latter option should be more appropriate for ex post production, because players do not need to be concerned with cooperation.
Investment Timing with Incentive-Disincentive Contracts under Asymmetric Information  [PDF]
Takashi Shibata, Michi Nishihara
Technology and Investment (TI) , 2012, DOI: 10.4236/ti.2012.32011
Abstract: This paper examines a manager’s investment timing in the presence of asymmetric information between an owner and the manager. In particular, we extend the asymmetric information problem by incorporating not only an incentive but also disincentive. Investment timing is delayed more under asymmetric information than under symmetric information. However, investment timing under asymmetric information converges to the symmetric information investment timing by making the disincentive (penalty) for the manager’s untruthful report sufficiently large. Consequently, by adopting an enlarged set of incentive-disincentive contracts framework, we showed that there is a relationship between the symmetric and asymmetric information problems.
GSE Is a Maternal Factor Involved in Active DNA Demethylation in Zygotes
Yuki Hatanaka, Natsumi Shimizu, Satoshi Nishikawa, Mikiko Tokoro, Seung-Wook Shin, Takuji Nishihara, Tomoko Amano, Masayuki Anzai, Hiromi Kato, Tasuku Mitani, Yoshihiko Hosoi, Satoshi Kishigami, Kazuya Matsumoto
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0060205
Abstract: After fertilization, the sperm and oocyte genomes undergo extensive epigenetic reprogramming to form a totipotent zygote. The dynamic epigenetic changes during early embryo development primarily involve DNA methylation and demethylation. We have previously identified Gse (gonad-specific expression gene) to be expressed specifically in germ cells and early embryos. Its encoded protein GSE is predominantly localized in the nuclei of cells from the zygote to blastocyst stages, suggesting possible roles in the epigenetic changes occurring during early embryo development. Here, we report the involvement of GSE in epigenetic reprogramming of the paternal genome during mouse zygote development. Preferential binding of GSE to the paternal chromatin was observed from pronuclear stage 2 (PN2) onward. A knockdown of GSE by antisense RNA in oocytes produced no apparent effect on the first and second cell cycles in preimplantation embryos, but caused a significant reduction in the loss of 5-methylcytosine (5 mC) and the accumulation of 5-hydroxymethylcytosine (5 hmC) in the paternal pronucleus. Furthermore, DNA methylation levels in CpG sites of LINE1 transposable elements, Lemd1, Nanog and the upstream regulatory region of the Oct4 (also known as Pou5f1) gene were clearly increased in GSE-knockdown zygotes at mid-pronuclear stages (PN3-4), but the imprinted H19-differential methylated region was not affected. Importantly, DNA immunoprecipitation of 5 mC and 5 hmC also indicates that knockdown of GSE in zygotes resulted in a significant reduction of the conversion of 5 mC to 5 hmC on LINE1. Therefore, our results suggest an important role of maternal GSE for mediating active DNA demethylation in the zygote.
Masashi Nishihara
Bijdragen tot de Taal-, Land- en Volkenkunde , 1988,
A Real Options Game Involving Multiple Projects
Michi Nishihara
Lecture Notes in Engineering and Computer Science , 2011,
Development of an Inflammation-Associated Colorectal Cancer Model and Its Application for Research on Carcinogenesis and Chemoprevention
Takuji Tanaka
International Journal of Inflammation , 2012, DOI: 10.1155/2012/658786
Abstract: Chronic inflammation is a well-recognized risk factor for development of human cancer in several tissues, including large bowel. Inflammatory bowel disease, including ulcerative colitis and Crohn’s disease, is a longstanding inflammatory disease of intestine with increased risk for colorectal cancer development. Several molecular events involved in chronic inflammatory process may contribute to multistep carcinogenesis of human colorectal cancer in the inflamed colon. They include overproduction of reactive oxygen and nitrogen species, overproduction and upregulation of productions and enzymes of arachidonic acid biosynthesis pathway and cytokines, and intestinal immune system dysfunction. In this paper, I will describe several methods to induce colorectal neoplasm in the inflamed colon. First, I will introduce a protocol of a novel inflammation-associated colon carcinogenesis in mice. In addition, powerful tumor-promotion/progression activity of dextran sodium sulfate in the large bowel of mice will be described. Finally, chemoprevention of inflammation-associated colon carcinogenesis will be mentioned. 1. Introduction Relationship between inflammation and cancer has been suggested for a long time [1]. Since Marshall and Warren [2], who discovered Helicobacter pylori and reported its infection closely associated with gastric cancer development, won the Nobel Prize in Physiology or Medicine in 2005, there have been an increasing number of reports on PubMed as to the relationship between inflammation and carcinogenesis in a variety of tissues (Table 1) and it has been featured in major journals. Table 1: Inflammation and cancer in various tissues. In terms of the large bowel, it has been found that the risk of colorectal cancer increases in relation to the degrees of inflammation and the disease duration (duration/risk = 10 years/1.6%, 20 years/8.3%, and 30 years/18.4%) in inflammatory bowl diseases (IBDs) such as ulcerative colitis (UC) and Crohn’s disease (CD) (Figure 1) [3]. I have been interested in inflammation-associated colorectal carcinogenesis for a long time, since even younger patients with UC have high risk of colorectal cancer [4]. Figure 1: UC patients are high-risk groups of colorectal cancer (CRC) development. Patients with UC as well as those with colorectal cancer have been increasing in Asian countries including Japan, similarly to Western countries (Figure 2) [5]. Therefore, it is necessary to investigate the mechanisms of colorectal cancer development with the background of inflammation for establishing the countermeasure strategy
Preclinical Cancer Chemoprevention Studies Using Animal Model of Inflammation-Associated Colorectal Carcinogenesis
Takuji Tanaka
Cancers , 2012, DOI: 10.3390/cancers4030673
Abstract: Inflammation is involved in all stages of carcinogenesis. Inflammatory bowel disease, such as ulcerative colitis and Crohn’s disease is a longstanding inflammatory disease of intestine with increased risk for colorectal cancer (CRC). Several molecular events involved in chronic inflammatory process are reported to contribute to multi-step carcinogenesis of CRC in the inflamed colon. They include over-production of free radicals, reactive oxygen and nitrogen species, up-regulation of inflammatory enzymes in arachidonic acid biosynthesis pathway, up-regulation of certain cytokines, and intestinal immune system dysfunction. In this article, firstly I briefly introduce our experimental animal models where colorectal neoplasms rapidly develop in the inflamed colorectum. Secondary, data on preclinical cancer chemoprevention studies of inflammation-associated colon carcinogenesis by morin, bezafibrate, and valproic acid, using this novel inflammation-related colorectal carcinogenesis model is described.
Message Routing Algorithm with Additional Node-Information for Capability-Aware Object Management in P2P Networks
Takuji Tachibana
Lecture Notes in Engineering and Computer Science , 2008,
Colorectal carcinogenesis: Review of human and experimental animal studies
Tanaka Takuji
Journal of Carcinogenesis , 2009,
Abstract: This review gives a comprehensive overview of cancer development and links it to the current understanding of tumorigenesis and malignant progression in colorectal cancer. The focus is on human and murine colorectal carcinogenesis and the histogenesis of this malignant disorder. A summary of a model of colitis-associated colon tumorigenesis (an AOM/DSS model) will also be presented. The earliest phases of colorectal oncogenesis occur in the normal mucosa, with a disorder of cell replication. The large majority of colorectal malignancies develop from an adenomatous polyp (adenoma). These can be defined as well-demarcated masses of epithelial dysplasia, with uncontrolled crypt cell proliferation. When neoplastic cells pass through the muscularis mucosa and infiltrate the submucosa, they are malignant. Carcinomas usually originate from pre-existing adenomas, but this does not imply that all polyps undergo malignant changes and does not exclude de novo oncogenesis. Besides adenomas, there are other types of pre-neoplasia, which include hyperplastic polyps, serrated adenomas, flat adenomas and dysplasia that occurs in the inflamed colon in associated with inflammatory bowel disease. Colorectal neoplasms cover a wide range of pre-malignant and malignant lesions, many of which can easily be removed during endoscopy if they are small. Colorectal neoplasms and/or pre-neoplasms can be prevented by interfering with the various steps of oncogenesis, which begins with uncontrolled epithelial cell replication, continues with the formation of adenomas and eventually evolves into malignancy. The knowledge described herein will help to reduce and prevent this malignancy, which is one of the most frequent neoplasms in some Western and developed countries.
Possibility of Unconventional Pairing Due to Coulomb Interaction in Fe-Based Pnictide Superconductors: Perturbative Analysis of Multi-Band Hubbard Models
Takuji Nomura
Physics , 2008, DOI: 10.1143/JPSJS.77SC.123
Abstract: Possibility of unconventional pairing due to Coulomb interaction in iron-pnictide superconductors is studied by applying a perturbative approach to realistic 2- and 5-band Hubbard models. The linearized Eliashberg equation is solved by expanding the effective pairing interaction perturbatively up to third order in the on-site Coulomb integrals. The numerical results for the 5-band model suggest that the eigenvalues of the Eliashberg equation are sufficiently large to explain the actual high Tc for realistic values of Coulomb interaction and the most probable pairing state is spin-singlet s-wave without any nodes just on the Fermi surfaces, although the superconducting order parameter changes its sign between the small Fermi pockets. On the other hand the 2-band model is quite insufficient to explain the actual high Tc.
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