Young-Ho Lee

Synergetic effect of copper-plating wastewater as a catalyst for the destruction of acrylonitrile wastewater in supercritical water oxidation.

A new supercritical water oxidation process for the simultaneous treatment of mixed wastewater containing wastewater from acrylonitrile manufacturing processes and copper-plating processes was investigated using a continuous tubular reactor system. Experiments were carried out at temperatures ranging from 400 to 600 degrees C and a pressure of 25 MPa. The residence time was fixed at 2s by changing the flow rates of feeds, depending on reaction temperature. The initial total organic carbon (TOC) concentration of the wastewaters and the O(2) concentration at the reactor inlet were kept constant at 0.49 and 0.74 mol/L. It was confirmed that the copper-plating wastewater accelerated the TOC conversion of acrylonitrile wastewater from 17.6% to 67.3% at a temperature of 450 degrees C. Moreover, copper and copper oxide nanoparticles were generated in the process of supercritical water oxidation (SCWO) of mixed wastewater. 99.8% of copper in mixed wastewater was recovered as solid copper and copper oxides at a temperature of 600 degrees C, with their average sizes ranging from 150 to 160 nm. Our study showed that SCWO provides a synergetic effect for simultaneous treatment of acrylonitrile and copper-plating wastewater. During the reaction, the oxidation rate of acrylonitrile wastewater was enhanced due to the in situ formation of nano-catalysts of copper and/or copper oxides, while the exothermic decomposition of acrylonitrile wastewater supplied enough heat for the recovery of solid copper and copper oxides from copper-plating wastewater. The synergetic effect of wastewater treatment by the newly proposed SCWO process leads to full TOC conversion, color removal, detoxification, and odor elimination, as well as full recovery of copper.

Fast and Accurate On-line Prediction of Performance and Power Consumption in Multicore-based Systems

Although multi-core processors have emerged as a dominant low-power architectural solution in high performance processor design, it is still challenging to take a full advantage of the high power efficiency of multi-core processors. One such challenge occurs when an operating system tries to assign a multi-threaded application to a target multi-core processor in an energy efficient fashion. With an increasing number of cores combined with sophisticated power management schemes, it becomes more difficult to decide the most appropriate runtime configuration for a given application so that the overall energy efficiency is maximized. In this paper, we propose a novel performance and power estimation technique, called PET, for multi-core systems. The PET scheme is based on a compact but accurate performance and power transformation model, which aims to predict the performance and power consumption of a large number of runtime configurations using hardware performance counters collected in a small number of representative runtime configurations. Using a transformation model, PET enables to accurately determine the best runtime configuration of multi-threaded applications at runtime with a small overhead over an existing naive solution. Experimental results on an Intel Q6600 quad-core processor show that PET can accurately predict the performance and power consumption of multi-threaded applications running on 1-4 cores under two different frequency levels with an average prediction error of 2.1%-8.3% and 3.2%-6.5% over the measured data, respectively. We also show that PET is effective in estimating the performance and power consumption of two co-running applications with an average prediction error of less than 5%.

Mitochondrial reprogramming via ATP5H loss promotes multimodal cancer therapy resistance

The host immune system plays a pivotal role in the emergence of tumor cells that are refractory to multiple clinical interventions including immunotherapy, chemotherapy, and radiotherapy. Here, we examined the molecular mechanisms by which the immune system triggers cross-resistance to these interventions. By examining the biological changes in murine and tumor cells subjected to sequential rounds of in vitro or in vivo immune selection via cognate cytotoxic T lymphocytes, we found that multimodality resistance arises through a core metabolic reprogramming pathway instigated by epigenetic loss of the ATP synthase subunit ATP5H, which leads to ROS accumulation and HIF-1&agr; stabilization under normoxia. Furthermore, this pathway confers to tumor cells a stem-like and invasive phenotype. In vivo delivery of antioxidants reverses these phenotypic changes and resensitizes tumor cells to therapy. ATP5H loss in the tumor is strongly linked to failure of therapy, disease progression, and poor survival in patients with cancer. Collectively, our results reveal a mechanism underlying immune-driven multimodality resistance to cancer therapy and demonstrate that rational targeting of mitochondrial metabolic reprogramming in tumor cells may overcome this resistance. We believe these results hold important implications for the clinical management of cancer.