A Practical Tessellation-Based Approach for Optimizing Cell-Specific Bias Values in LTE-A Heterogeneous Cellular Networks

In order to implement an optimized solution for cell range expansion (CRE) and enhanced intercell interference coordination (eICIC) schemes in long-term evolution-advanced (LTE-A) heterogeneous cellular networks (HCNs) and to realize good load-balancing performance in existing LTE-A systems, a practical tessellation-based algorithm is proposed. In this algorithm, a globalized cell-specific bias optimization and a localized almost blank subframe (ABS) ratio update are proposed. The proposed scheme does not require major changes to existing protocols. Thus, it can be implemented in existing LTE-A systems with any legacy user equipment (UE) with only a partial update to the BSs and core networks. From simulation results, it is shown that the tessellation formed by the proposed approach is quite consistent with the optimal one for various realistic scenarios. Thus, the proposed scheme can provide a much better load-balancing capability compared with the conventional common bias scheme. Owing to the improved load-balancing capability, the user rate distribution of the proposed scheme is much better than that obtained from the conventional scheme and is even indistinguishable from that of the ideal joint user association scheme

User Detection Performance Analysis for Grant-Free Uplink Transmission in Large-Scale Antenna Systems

In this paper, user detection performance of a grant-free uplink transmission in a large scale antenna system is analyzed, in which a general grant-free multiple access is considered as the system model and Zadoff-Chu sequence is used for the uplink pilot. The false alarm probabilities of various user detection schemes under the target detection probabilities are evaluated

DETERMINATION OF LINEAR AND NONLINEAR ROLL DAMPING COEFFICIENTS OF A SHIP SECTION USING CFD

The most prevalently used method to obtain the nonlinear roll damping coefficient is the free roll decay test. However, this method can only be conducted at the resonance frequency and thus cannot consider the effect of the frequency. This is a certain limitation as the resonance frequency can be changed at any time by the ship’s loading conditions. Therefore, it is worth investigating the frequency dependency of the nonlinear roll damping coefficients. In this study, a numerical method was proposed to derive the linear and nonlinear roll damping coefficients of ships at different frequencies. Fully nonlinear CFD simulations of forced harmonic roll motion were conducted and the roll damping coefficients were calculated. Then, the damping coefficients were decomposed into the linear and nonlinear components using the linear regression analysis. The linear roll damping coefficients were compared with potential coefficients and showed a good agreement, while the nonlinear roll damping coefficients were compared with the coefficients calculated using a semi-empirical method. The nonlinear roll damping coefficients calculated from the proposed method showed a strong frequency dependency. Finally, possible rationales for the frequency dependence of the nonlinear roll damping coefficient were investigated

Sink-Independent Model in Wireless Sensor Networks

Wireless sensor networks generally support users that send queries and receive data via the sinks. The user and the sinks are mostly connected to each other by infrastructure networks. The users, however, should receive the data from the sinks through multi-hop communications between disseminating sensor nodes if such users move into the sensor networks without infrastructure networks. To support mobile users, previous work has studied various user mobility models. Nevertheless, such approaches are not compatible with the existing routing algorithms, and it is difficult for the mobile users to gather data efficiently due to their mobility. To improve the shortcomings, we propose a view of mobility for wireless sensor networks and propose a model to support a user mobility that is independent of sinks

Study of Analyzing Outcome of Building and Introducing System for Preserving Full-Text of e-Journal

Today, most researchers conduct their studies through the full-text of e-journals. Therefore, an important base for domestic development of science and technology is to obtain the full-text of quality e-journals by overseas researchers and to provide it to Korea's researchers. This study aims to build a system based on the National Archiving Center for the full-text of e-journals and to make a service system for providing them to the public by acquiring the full-text of quality overseas e-journals. To do this, an analysis was made of the outcome of introducing such a system for full-text of e-journals in comparison with the investment. As a result, 112 more institutions, that is, from 47 institutions to 159 institutions, have introduced the system as of 2012, and the number of downloaded full-texts increased at least 2.17 times

Gelatin-layered and multi-sized porous β-tricalcium phosphate for tissue engineering scaffold

The multi-sized porous β-tricalcium phosphate scaffolds were fabricated by freeze drying followed by slurry coating using a multi-sized porous sponge as a template. Then, gelatin was dip coated on the multi-sized porous β-tricalcium phosphate scaffolds under vacuum. The mechanical and biological properties of the fabricated scaffolds were evaluated and compared to the uniformly sized porous scaffolds and scaffolds that were not coated by gelatin. The compressive strength was tested by a universal testing machine, and the cell viability and differentiation behavior were measured using a cell counting kit and alkaline phosphatase activity using the MC3T3-E1 cells. In comparison, the gelatin-coated multi-sized porous β-tricalcium phosphate scaffold showed enhanced compressive strength. After 14 days, the multi-sized pores were shown to affect cell differentiation, and gelatin coatings were shown to affect the cell viability and differentiation. The results of this study demonstrated that the multi-sized porous β-tricalcium phosphate scaffold coated by gelatin enhanced the mechanical and biological strengths

Inhibition of autophagy promotes salinomycin-induced apoptosis via reactive oxygen species-mediated PI3K/AKT/mTOR and ERK/p38 MAPK-dependent signaling in human prostate cancer cells

Recently, the interplay between autophagy and apoptosis has become an important factor in chemotherapy for cancer treatment. Inhibition of autophagy may be an effective strategy to improve the treatment of chemo-resistant cancer by consistent exposure to chemotherapeutic drugs. However, no reports have clearly elucidated the underlying mechanisms. Therefore, in this study, we assessed whether salinomycin, a promising anticancer drug, induces apoptosis and elucidated potential antitumor mechanisms in chemo-resistant prostate cancer cells. Cell viability assay, Western blot, annexin V/propidium iodide assay, acridine orange (AO) staining, caspase-3 activity assay, reactive oxygen species (ROS) production, and mitochondrial membrane potential were assayed. Our data showed that salinomycin alters the sensitivity of prostate cancer cells to autophagy. Pretreatment with 3-methyladenine (3-MA), an autophagy inhibitor, enhanced the salinomycin-induced apoptosis. Notably, salinomycin decreased phosphorylated of AKT and phosphorylated mammalian target of rapamycin (mTOR) in prostate cancer cells. Pretreatment with LY294002, an autophagy and PI3K inhibitor, enhanced the salinomycin-induced apoptosis by decreasing the AKT and mTOR activities and suppressing autophagy. However, pretreatment with PD98059 and SB203580, an extracellular signal-regulated kinases (ERK), and p38 inhibitors, suppressed the salinomycin-induced autophagy by reversing the upregulation of ERK and p38. In addition, pretreatment with N-acetyl-L-cysteine (NAC), an antioxidant, inhibited salinomycin-induced autophagy by suppressing ROS production. Our results suggested that salinomycin induces apoptosis, which was related to ROS-mediated autophagy through regulation of the PI3K/AKT/mTOR and ERK/p38 MAPK signaling pathways