著者
Hasegawa K. Umemura M.
出版者
Wiley-Blackwell
雑誌
Monthly notices of the Royal Astronomical Society (ISSN:00358711)
巻号頁・発行日
vol.407, no.4, pp.2632-2644, 2010-10
被引用文献数
21 11

We present a novel radiation hydrodynamics code, start, which is a smoothed particle hydrodynamics (SPH) scheme coupled with accelerated radiative transfer. The basic idea for the acceleration of radiative transfer is parallel to the tree algorithm that is hitherto used to speed up the gravitational force calculation in an N-body system. It is demonstrated that the radiative transfer calculations can be dramatically accelerated, where the computational time is scaled as Np log Ns for Np SPH particles and Ns radiation sources. Such acceleration allows us to readily include not only numerous sources but also scattering photons, even if the total number of radiation sources is comparable to that of SPH particles. Here, a test simulation is presented for a multiple source problem, where the results with start are compared to those with a radiation SPH code without tree-based acceleration. We find that the results agree well with each other if we set the tolerance parameter as θcrit≤ 1.0, and then it demonstrates that start can solve radiative transfer faster without reducing the accuracy. One of the important applications with start is to solve the transfer of diffuse ionizing photons, where each SPH particle is regarded as an emitter. To illustrate the competence of start, we simulate the shadowing effect by dense clumps around an ionizing source. As a result, it is found that the erosion of shadows by diffuse recombination photons can be solved. Such an effect is of great significance to reveal the cosmic reionization process.
著者
Yang Weiwen Itoh Fumiko Ohya Hirotoshi Kishimoto Fukiko Tanaka Aya Nakano Naoko Itoh Susumu Kato Mitsuyasu
出版者
Wiley-Blackwell
雑誌
Cancer science (ISSN:13479032)
巻号頁・発行日
vol.102, no.10, pp.1808-1814, 2011-10
被引用文献数
8 2

he basic helix–loop–helix protein E2-2 is known to play a role in quiescence of endothelial cells (ECs). However, it is unclear how the activity of E2-2 is controlled in the cells. In this study, we identified FAM96B as an interaction partner of E2-2. FAM96B interfered with E2-2-mediated effects on luciferase reporter activities. Furthermore, the suppression of vascular endothelial growth factor receptor 2 promoter activity by E2-2 was rescued by the expression of FAM96B in a dose-dependent manner. Interestingly, FAM96B decreased the expression of ectopic and endogenous E2-2 proteins. Mutational analysis revealed that the middle region of FAM96B is required for the limited expression of E2-2 protein. When FAM96B was expressed in ECs, the EC migration, proliferation, and tube formation were potentiated. Taken together, these findings suggest that FAM96B acts as a regulator of E2-2 through the control of its protein expression.