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.

Ab initio study of field emission from graphitic ribbons.

Abstract: We have performed first-principles calculations on field emission (FE) from graphitic ribbons within the time-dependent density-functional theory. An important finding is that dangling bond states localized at clean edges are major contributors to FE current. H termination makes the FE current small due to the disappearance of the dangling-bond states. FE is found not to occur from the edge state of a H-terminated zigzag ribbon even when the state is at the Fermi level. The results of the FE current from graphitic ribbons give approximately 1 microA for maximum of FE current from a circular edge of graphitic sheets with approximately 1 nm diameter of an open-ended multiwalled carbon nanotube under a high electric field of approximately 1 V/A.

Stabilization in a chemotaxis model for tumor invasion

Abstract: This paper deals with the chemotaxis system \[ \begin{cases} u_t=\Delta u - abla \cdot (u abla v), \qquad x\in \Omega, \ t>0, \\ v_t=\Delta v + wz, \qquad x\in \Omega, \ t>0, \\ w_t=-wz, \qquad x\in \Omega, \ t>0, \\ z_t=\Delta z - z + u, \qquad x\in \Omega, \ t>0, \end{cases} \] in a smoothly bounded domain $\Omega \subset \mathbb{R}^n$, $n \le 3$, that has recently been proposed as a model for tumor invasion in which the role of an active extracellular matrix is accounted for. It is shown that for any choice of nonnegative and suitably regular initial data $(u_0,v_0,w_0,z_0)$, a corresponding initial-boundary value problem of Neumann type possesses a global solution which is bounded. Moreover, it is proved that whenever $u_0 ot\equiv 0$, these solutions approach a certain spatially homogeneous equilibrium in the sense that as $t\to\infty$, $u(x,t)\to \overline{u_0}$ ,   $v(x,t) \to \overline{v_0} + \overline{w_0}$,   $w(x,t) \to 0$   and   $z(x,t) \to \overline{u_0}$,   uniformly with respect to $x\in\Omega$, where $\overline{u_0}:=\frac{1}{|\Omega|} \int_{\Omega} u_0$, $\overline{v_0}:=\frac{1}{|\Omega|} \int_{\Omega} v_0$  and   $\overline{w_0}:=\frac{1}{|\Omega|} \int_{\Omega} w_0$.

Nickel-Catalyzed Intermolecular [3 + 2 + 2] Cocyclization of Ethyl Cyclopropylideneacetate and Alkynes

Abstract: The [3 + 2 + 2] cocyclization of ethyl cyclopropylideneacetate (1a) and terminal alkynes (2) proceeded smoothly in the presence of 10 mol % “Ni(PPh3)2”, which was prepared in situ from Ni(cod)2 and PPh3. The high reactivity of 1a, which was induced by the introduction of an electron-withdrawing group, is very important for the progress of this reaction. The cycloheptadiene derivatives were synthesized in highly selective manner in good yields.

CCR5 is a suppressor for cortical plasticity and hippocampal learning and memory

Abstract: Although the role of CCR5 in immunity and in HIV infection has been studied widely, its role in neuronal plasticity, learning and memory is not understood. Here, we report that decreasing the function of CCR5 increases MAPK/CREB signaling, long-term potentiation (LTP), and hippocampus-dependent memory in mice, while neuronal CCR5 overexpression caused memory deficits. Decreasing CCR5 function in mouse barrel cortex also resulted in enhanced spike timing dependent plasticity and consequently, dramatically accelerated experience-dependent plasticity. These results suggest that CCR5 is a powerful suppressor for plasticity and memory, and CCR5 over-activation by viral proteins may contribute to HIV-associated cognitive deficits. Consistent with this hypothesis, the HIV V3 peptide caused LTP, signaling and memory deficits that were prevented by Ccr5 knockout or knockdown. Overall, our results demonstrate that CCR5 plays an important role in neuroplasticity, learning and memory, and indicate that CCR5 has a role in the cognitive deficits caused by HIV.

Basophil-derived IL-4 promotes epicutaneous antigen sensitization concomitant with the development of food allergy

Abstract: Background Exaggerated thymic stromal lymphopoietin (TSLP) production and infiltration of basophils are associated with the pathogenesis of atopic dermatitis (AD), a recognized risk factor for the development of food allergies. Although TSLP and basophils have been implicated in promotion of food-induced allergic disorders in response to epicutaneous sensitization, the mechanisms by which TSLP-elicited basophils guide the progression of allergic inflammation in the skin to distant mucosal sites, such as the gastrointestinal tract, are poorly understood. Objective We sought to test the role of basophil-intrinsic IL-4 production in TH2 sensitization to food antigens in the skin and effector food-induced allergic responses in the gut. Methods Mice were epicutaneously sensitized with ovalbumin on an AD-like skin lesion, followed by intragastric antigen challenge to induce IgE-mediated food allergy. The requirement for basophil-derived IL-4 production for TH2 polarization and the pathogenesis of IgE-mediated food allergy was assessed in vitro by using coculture experiments with naive T cells and in vivo by using Il4 3′UTR mice that selectively lack IL-4 production in basophils. Results Epicutaneous food antigen sensitization is associated with infiltration of IL-4–competent innate immune cells to the skin, with basophils and eosinophils representing the predominant populations. In contrast to basophils, absence of eosinophils did not alter disease outcome. Coculture of IL-4–competent basophils together with dendritic cells and naive T cells was sufficient to promote TH2 polarization in an IL-4–dependent manner in vitro, whereas absence of basophil-intrinsic IL-4 production in vivo was associated with reduced food-induced allergic responses. Conclusion TSLP-elicited basophils promote epicutaneous sensitization to food antigens and subsequent IgE-mediated food allergy through IL-4. Strategies to target the TSLP–basophil–IL-4 axis in patients with AD might lead to innovative therapies that can prevent the progression of allergies to distant mucosal sites.