Chung-Ang University

About: Chung-Ang University is a education organization based out in Seoul, South Korea. It is known for research contribution in the topics: Population & Thin film. The organization has 13381 authors who have published 26978 publications receiving 416735 citations. The organization is also known as: CAU & Chung.

Anomalous Thermal Conductivity and Magnetic Torque Response in the Honeycomb Magnet α − RuCl 3

Abstract: We report on the unusual behavior of the in-plane thermal conductivity $\ensuremath{\kappa}$ and torque $\ensuremath{\tau}$ response in the Kitaev-Heisenberg material $\ensuremath{\alpha}\text{\ensuremath{-}}{\mathrm{RuCl}}_{3}$. $\ensuremath{\kappa}$ shows a striking enhancement with linear growth beyond $H=7\text{ }\text{ }\mathrm{T}$, where magnetic order disappears, while $\ensuremath{\tau}$ for both of the in-plane symmetry directions shows an anomaly at the same field. The temperature and field dependence of $\ensuremath{\kappa}$ are far more complex than conventional phonon and magnon contributions, and require us to invoke the presence of unconventional spin excitations whose properties are characteristic of a field-induced spin-liquid phase related to the enigmatic physics of the Kitaev model in an applied magnetic field.

Exploring immersive experience in journalism

Abstract: Although virtual reality (VR) has been widely used to deliver news stories in immersive journalism (IJ), it is not clear how people are actually experiencing these stories and their contexts. Focusing on the immersion feature of VR stories, this study explicates the user experience to determine what it is like to experience news stories in VR and how immersion improves viewing experiences in IJ. This study proposes a VR experience model in the IJ context that integrates cognitive, affective, and behavioral factors as the primary influencing determinants. The results indicate that the meaning of immersion strongly depends on the users’ traits and contexts and that the function of immersion is strongly determined by the users’ own cognition and intentions. VR stories are viewed and accepted based on the manner that users imagine and intend to experience them. The model demonstrates the users’ cognitive processes of experiencing quality, value, and satisfaction, which determine how people empathize with and ...

Chloromethyl ketones block induction of nitric oxide synthase in murine macrophages by preventing activation of nuclear factor-kappa B.

Abstract: N-alpha-tosyl-L-phenylalanine chloromethyl ketone (TPCK) and N-alpha-tosyl-L-lysine chloromethyl ketone (TLCK), serine protease inhibitors, block many cytotoxic functions of immune cells including superoxide anion production, cytokine release, cell-mediated cytolysis, and nitric oxide (NO)-related macrophage functions. IFN-gamma/LPS-induced NO production from murine peritoneal macrophages was inhibited by TPCK and TLCK in a dose-dependent manner (EC50s: approximately 20 microM for TPCK and approximately 30 microM for TLCK). Viability exceeded 91% with 25 microM TPCK and with 80 microM TLCK. When TPCK treatment was delayed until 1 h of activation, the inhibitory effect was markedly reduced. After 2 h of the activation, TPCK was not effective anymore. Addition of either TNF-alpha or conditioned media from IFN-gamma/LPS-activated macrophage culture did not prevent the inhibitory effect of TPCK. Neither TPCK nor TLCK reduced enzymatic NO production from macrophage lysates. Lysates from TPCK-treated cells did not generate NO even after supplementing necessary cofactors for NO synthase. Immunoblotting analysis showed that simultaneous treatment of TPCK with IFN-gamma/LPS abolished the NO synthase expression, whereas delayed addition of TPCK was either partially effective or not effective at all. Furthermore, TPCK treatment reduced the concentration of mRNA for NO synthase without decreasing mRNA stability. Thus, the serine protease inhibitors directly blocked an early event in expression of NO synthase. Electrophoretic mobility shift assay indicated that TPCK blocked the activation of nuclear factor-kappa B, a transcription factor necessary for NO synthase induction. TPCK also blocked disappearance of I kappa B from cytosolic fraction, and nuclear translocation of NF-kappa B subunits p50 and p65. Delaying the addition of TPCK by 10 min partially prevented the inhibition of the NF-kappa B activation process and allowed partial resuming of NO production. Thus, TPCK inhibited NO synthase induction by blocking NF-kappa B activation.