• The Journal of Korean Institute of Communications and Information Sciences
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• v.33 no.11A
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• pp.1021-1033
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• 2008

In recent years, the growing interest in wireless sensor network has resulted in thousands of publications. Most of this research is concerned with delivering raw data such as temperature, pressure, or humidity. Recently, the focus of sensor network paradigm is changing for delivering multimedia contents. However, most existing routing protocols are not very practical for transmitting multimedia contents in resource constrained sensor networks. In this paper, we propose an optimized node-disjoint multi-path routing protocol for throughput enhancement and load balancing. We focused on how to allocate traffic to independent multiple end-to-end routes. Decentralized transmission using our node-disjoint multi-path routing scheme results in bandwidth aggregation and throughput enhancement. In addition, our scheme provides ways to remove link-joint routes for decreasing routing overhead.

• Journal of the Korea Society for Simulation
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• v.17 no.3
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• pp.1-8
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• 2008

It is essential to maintain constant QoS despite of cell overload or erroneous wireless link during transmission because QoS of a multimedia service may be severely degraded by small delay or packet loss. This paper deals with a cell selection method for supporting the QoS of multimedia services over heterogeneous networks. The proposed scheme is based on Fuzzy Multi-Criteria Decision Making (FMCDM), in which uncertain parameters such as user system preference, the communication cost and cell load, and the transmission delay are used in the decision process using the aggregation function in fuzzy set theory. In this scheme, errors in the evaluation parameters impose milder changes on the total evaluation value than in binary logics. Simulation is focused on the average delay and packet loss rate, and the simulation results show that our proposed method provides mobile terminals the optimal performance.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.32 no.3
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• pp.218-228
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• 2010

Components of dental resin-based restorative materials are reported to leach from the filling materials even after polymerization. Hydroquinone (HQ) is one of the major monomers used in the dental resin and is known as a carcinogen. Thus, carcinogenic risk of HQ leaching from the dental resin becomes a public health concern. The present study attempted to examine the carcinogenic potentials of HQ on the human epithelial cell, which is the target cell origin of the most of oral cancers. Cytotoxicity of HQ was observed above 50${\mu}M$ as measured by LDH assay, indicating a relatively low toxicity of this substance in human epithelial cells. The parameters of neoplastic cellular transformation such as cell saturation density, soft agar colony formation and cell aggregation were analyzed to examine the carcinogenic potential of HQ. The study showed that 2-week exposure of HQ showed the tendency of increase in the saturation density and the significant enhancement of soft agar colony formation at the highest dose, 50 ${\mu}M$ only. It is suggested that HQ has a weak potential of carcinogenicity. When cells were treated with HQ and TPA, a well-known tumor promoter, the parameters of neoplastic cellular transformation was significantly increased. This result indicates that the potential risk of carcinogenicity from HQ is largely dependent upon the presence of promoter. Exposure of 50 ${\mu}M$ HQ increased the time-dependent apoptosis as measured by the ELISA kit. This concentration coincides with a dose of neoplastic transformation, indicating a possible link between apoptosis and HQ-induced cellular transformation. Hydroquinone generated Reactive Oxygen Species (ROS) which was evidenced by the treatment of antioxidants such as trolox and N-acetyl cysteine and the GSH depleting agent, BSO. Antioxidants blocked the generation of ROS and the GSH depleting agent, BSO dramatically increased the ROS production. Since HQ is known to increase ROS production thru activation of transcriptional factor such as c-Myb and Pim-1, it is speculated that ROS generation by HQ plays a role in the activation of oncogene, which may lead to neoplastic transformation. In addition, ROS is involved in the alteration of signal transduction, which regulates the apoptosis in many cellular systems. Thus, ROS-mediated apoptosis may be involved in the HQ-induced carcinogenic processes. Protein kinase C (PKC) is known to play pivotal roles in neoplastic transformation of cells and its high expression is often found in a variety of types of tumors including oral cancer. PKC translocation of PKC-${\alpha}$ was observed following HQ exposure. Altered signaling system may also play a role in the transformation process. Taken together, HQ leached from the dental resin does not pose a significant threat as a cancer causing agent, but its carcinogenic potential can be significantly elevated in the presence of promoter. The mechanism of HQ-induced carcinogenesis involved ROS generation, apoptosis and altered signaling pathway. The present study will provide a valuable data to estimate the potential risk of HQ as a carcinogen and understand mechanism of HQ-induced carcinogenesis in human epithelial cells.