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Articles by Yongjun Zhang
Total Records ( 2 ) for Yongjun Zhang
  Yongjun Zhang , Guoying Wei , Zimin Zhang , Tianrang Jia and Dengfeng Yang
  For coal seams susceptible to serious coal and gas outburst, numerous problems and issues, such as the low excavation speed and serious security risks, exist during the process of outburst prevention. Through on-site examinations, this study analyzes the effect of hydraulic slotting measures on changes in the coal-bearing assemblages and gas status and reveals the involved mechanisms that hydraulic slotting measures are applied to deal with coal and gas outburst. This study further proposes the rapid excavation technology with supporting equipment designed and integrated and establishes a comprehensive security system with hydraulic slotting as the core of the entire system. Therefore, the goals of achieving hydraulic slotting operated unattended to avoid personnel injury, implementing coal and gas control technology are achieved. The results of on-site examination indicate that the excavation speed using the proposed method could be two times faster than the excavation speed when boring and drilling method is applied and thus the goal of safely and efficiently carrying out excavation work in coal seams with severe coal and gas outburst potentials is realized.
  Ka Chen , Yizeng Tu , Yongjun Zhang , Harry C. Blair , Lin Zhang and Chuanyue Wu
  Resistance to apoptosis is a hallmark of cancer cells. We report here that PINCH-1, a cytoplasmic component of cell-extracellular matrix adhesions, is required for protection of multiple types of cancer cells from apoptosis. Furthermore, using HT-1080 fibrosarcoma cells as a model system, we have investigated the signaling pathway through which PINCH-1 contributes to apoptosis resistance. Loss of PINCH-1 markedly increases the level of Bim and promotes Bim translocation to mitochondria, resulting in activation of the intrinsic apoptosis pathway. Depletion of Bim completely blocked apoptosis induced by the loss of PINCH-1. Thus, PINCH-1 contributes to apoptosis resistance through suppression of Bim. Mechanistically, PINCH-1 suppresses Bim not only transcriptionally but also post-transcriptionally. PINCH-1 promotes activating phosphorylation of Src family kinase and ERK1/2. Consistent with this, ERK1/2-mediated Ser69 phosphorylation of Bim, a key signal for turnover of Bim, is suppressed by the removal of PINCH-1. Our results demonstrate a strong dependence of multiple types of apoptosis-resistant cancer cells on PINCH-1 and provide new insights into the molecular mechanism by which cancer cells are protected from apoptosis.

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