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( Jing Duan ),( Jidong Liang ),( Yiping Wang ),( Wenjing Du ),( Dongqi Wang ) 한국미생물 · 생명공학회 2016 Journal of microbiology and biotechnology Vol.26 No.10
Wastewater containing kraft lignin (KL) discharged from pulp and paper industries could cause serious environmental contamination. Appropriate effluent treatment is required to reduce the pollution. Investigations on anaerobic bacteria capable of degrading KL are beneficial to both lignin removal and biofuel regeneration from the effluent. In this paper, an anaerobic strain capable of degrading KL was isolated from the sludge of a pulp and paper mill and identified as Dysgonomonas sp. WJDL-Y1 by 16S rRNA analysis. Optimum conditions for KL degradation by strain WJDL-Y1 were obtained at initial pH of 6.8, C:N ratio of 6 and temperature of 33°C, based on statistical analyses by response surface methodology. For a 1.2 g/l KL solution, a COD removal rate of 20.7% concomitant with biomass increase of 17.6% was achieved after 4 days of incubation under the optimum conditions. After the treatment by strain WJDL-Y1, KL was modified and degraded.
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Hui Sun,Yingzi Liang,Yuning Wang,Xiangcheng Liu,Jidong Chen 대한토목학회 2021 KSCE JOURNAL OF CIVIL ENGINEERING Vol.25 No.10
Build-Operate-Transfer (BOT) plays a significant part in promoting the construction of freeways. Due to the long construction period and large investment, many uncertain factors affect the inputs, outputs, and returns of freeway projects during the construction and operation periods. For project investments, funds, returns, risks, and other relevant factors of the projects should be considered, evaluated, and balanced. This paper presents the perception of net present value (NPV) at risk to solve the uncertain financing parameters of BOT freeway project. This paper analyses the critical indicators of BOT project investment, and establishes an investment portfolio decision-making model for BOT freeway projects to maximize the NPV of the project portfolio. Based on the proposed model, this paper calculates the optimal investment portfolio with real constraints from financial perspective. At last, an investment portfolio case study is also provided to test the proposed model.
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MACC1 Expression Correlates with PFKFB2 and Survival in Hepatocellular Carcinoma
Ji, Dong,Lu, Zhong-Tang,Li, Yao-Qing,Liang, Zhe-Yong,Zhang, Peng-Fei,Li, Chao,Zhang, Jun-Li,Zheng, Xin,Yao, Ying-Min Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.2
Objective: To validate the relationship between MACC1 and 6-phosphofructo-2-kinase/fructose 2, 6 bisphosphatase (PFKFB2) expression as well as its clinicopathological features and prognostic significance in hepatocellular carcinoma. Methods: By using immunohistochemistry, we investigated the MACC1 and PFKFB2 protein expression in 60 pairs of hepatocellular carcinoma and corresponding non-tumor tissues. Using the Mann-Whitney U test, the Chi-square test, Kaplan-Meier survival analysis, Cox proportional hazard regression analysis and Spearman analysis, we studied the relationship between MACC1 and PFKFB2 protein expression and postoperative overall survival (OS) of the HCC patients. Results: MACC1 and PFKFB2 positive staining rates were significantly higher in hepatocellular carcinoma than in the corresponding nontumor tissues (P=0.012 and 0.04, respectively). The clinicopathological features evaluation revealed that positive expression of MACC1 was associated with a high Edmondson classification (P=0.007) and advanced TNM stage (P=0.027). Similar findings were evident for PFKFB2 expression (P=0.002 and P=0.027). MACC1 and PFKFB2 positive expression was associated with a lower OS rate (P=0.004 and 0.03, respectively). Kaplan-Meier survival and Cox proportional hazard regression analyses revealed MACC1 positive expression to be a prognostic factor for postoperative OS, but PFKFB was not. Conclusion: Highly expressed MACC1 and PFKFB2 protein were associated with TNM stage, Edmondson-Steier classification and overall survival. MACC1 may affect tumor metabolism partly through expression and phophorylation of PFKFB2.
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