Tokyo University of Science

About: Tokyo University of Science is a education organization based out in Tokyo, Japan. It is known for research contribution in the topics: Catalysis & Thin film. The organization has 15800 authors who have published 24147 publications receiving 438081 citations. The organization is also known as: Tōkyō Rika Daigaku & Science University of Tokyo.

Protective neutralizing influenza antibody response in the absence of T follicular helper cells

Abstract: Virus infection induces the development of T follicular helper (TFH) and T helper 1 (TH1) cells Although TFH cells are important in anti-viral humoral immunity, the contribution of TH1 cells to a protective antibody response remains unknown We found that IgG2 antibodies predominated in the response to vaccination with inactivated influenza A virus (IAV) and were responsible for protective immunity to lethal challenge with pathogenic H5N1 and pandemic H1N1 IAV strains, even in mice that lacked TFH cells and germinal centers The cytokines interleukin-21 and interferon-γ, which are secreted from TH1 cells, were essential for the observed greater persistence and higher titers of IgG2 protective antibodies Our results suggest that TH1 induction could be a promising strategy for producing effective neutralizing antibodies against emerging influenza viruses

Investigation of the TiN Gate Electrode With Tunable Work Function and Its Application for FinFET Fabrication

Abstract: The titanium nitride (TiN) gate electrode with a tunable work function has successfully been deposited on the sidewalls of upstanding Si-fin channels of FinFETs by using a conventional reactive sputtering. It was found that the work function of the TiN (phiTiN) slightly decreases with increasing nitrogen (N2) gas flow ratio, RN=N2/(Ar+N2) in the sputtering, from 17% to 100%. The experimental threshold voltage (Vth) dependence on the RN shows that the more RN offers the lower Vth for the TiN gate n-channel FinFETs. The composition analysis of the TiN films with different RN showed that the more amount of nitrogen is introduced into the TiN films with increasing RN, which suggests that the lowering of phi TiN with increasing RN should be related to the increase in nitrogen concentration in the TiN film. The desirable Vth shift from -0.22 to 0.22 V was experimentally confirmed by fabricating n+ poly-Si and TiN gate n-channel multi-FinFETs without a channel doping. The developed simple technique for the conformal TiN deposition on the sidewalls of Si-fin channels is very attractive to the TiN gate FinFET fabrication

Autocrine regulation of TGF-β1-induced cell migration by exocytosis of ATP and activation of P2 receptors in human lung cancer cells.

Abstract: Summary TGF-β1 plays a key role in cancer progression through induction of various biological effects, including cell migration. Extracellular nucleotides, such as ATP, released from cells play a role in signaling through activation of P2 receptors. We show here that exocytosis of ATP followed by activation of P2 receptors play a key role in TGF-β1-induced actin remodeling associated with cell migration. Treatment with TGF-β1 facilitated migration of human lung cancer A549 cells, which was blocked by pretreatment with ecto-nucleotidase and P2 receptor antagonists. ATP and P2 agonists facilitated cell migration. TGF-β1-induced actin remodeling, which contributes to cell migration, was also suppressed by pretreatment with ecto-nucleotidase and P2 receptor antagonists. Knockdown of P2X7 receptor suppressed TGF-β1-induced migration and actin remodeling. These results indicate the involvement of TGF-β1-induced ATP release in cell migration, at least in part, through activation of P2X7 receptors. TGF-β1 caused release of ATP from A549 cells within 10 minutes. Both ATP-enriched vesicles and expression of a vesicular nucleotide transporter (VNUT) SLC17A9, which is responsible for exocytosis of ATP, were found in cytosol of A549 cells. TGF-β1 failed to induce release of ATP from SLC17A9-knockdown cells. TGF-β1-induced cell migration and actin remodeling were also decreased in SLC17A9-knockdown cells. These results suggest the importance of exocytosis of ATP in cell migration. We conclude that autocrine signaling through exocytosis of ATP and activation of P2 receptors is required for the amplification of TGF-β1-induced migration of lung cancer cells.

A simple algorithm to compute comprehensive Gröbner bases using Gröbner bases

Abstract: We introduce a simple algorithm to compute comprehensive Grobner bases. It requires only computations of reduced Grobner bases in polynomial rings over ground fields. It is so simple that we can easily implement it on any computer algebra system that has a routine to compute reduced Grobner bases. Our implementations on several computer algebra systems show that it is also sufficiently fast comparing with other existing algorithms.