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Boa Nam,Jeonghwan Kim,Nahyeon Kim,Soondo Hong 대한산업공학회 2015 대한산업공학회 추계학술대회논문집 Vol.2015 No.11
This paper discusses a Discrete Time Markov Chain (DTMC) model to analyze the walks, picks, and blocked states of two workers in a wide aisle circular-passage system. We develop a DTMC model when two workers pass one pick face with half of unit pick time, and derive the throughput loss model in a closed-form expression. We test the model with a simulation study to determine how the passing allowance assumption can improve operational throughput. The results show that the avoidance delay while passing impacts the throughput. We believe that the analytical model is an important step in developing a general blocking model in a wide aisle circular-passage system.
Kim, Ji Hye,Nam, Boas,Choi, Yun Jung,Kim, Seon Ye,Lee, Jung-Eun,Sung, Ki Jung,Kim, Woo Sung,Choi, Chang-Min,Chang, Eun-Ju,Koh, Jae Soo,Song, Joon Seon,Yoon, Shinkyo,Lee, Jae Cheol,Rho, Jin Kyung,Son, American Association for Cancer Research 2018 Cancer Research Vol.78 No.16
<P>Enhanced glycolysis by EGFR mutation is required for maintaining EGFR levels via inhibition of JNK-induced autophagy. This provides a promising rationale for use of JNK activators in patients with EGFR-mutated NSCLC.</P><P>Oncogenic EGFR is essential for the development and growth of non–small cell lung cancer (NSCLC), but the precise roles of EGFR in lung cancer metabolism remain unclear. Here, we show that EGFR mutation-mediated enhancement of glycolysis is critical for EGFR stability. EGFR knockdown significantly decreased levels of glycolytic pathway intermediates via transcriptional regulation of glycolytic genes. EGFR mutation-enhanced glycolysis was required for fueling the tricarboxylic acid cycle, a critical component of EGFR stability. Nonsustained ATP production enhanced reactive oxygen species accumulation and subsequent JNK-mediated activation of autophagy, which in turn induced EGFR degradation. Our data show that EGFR-mutant NSCLCs require EGFR mutation-enhanced glycolysis to maintain EGFR stability. This pathway may serve as an attractive therapeutic target for EGFR-mutant NSCLCs.</P><P><B>Significance:</B> Enhanced glycolysis by EGFR mutation is required for maintaining EGFR levels via inhibition of JNK-induced autophagy. This provides a promising rationale for use of JNK activators in patients with EGFR-mutated NSCLC. <I>Cancer Res; 78(16); 4482–96. ©2018 AACR</I>.</P>