某焦化场地土壤中多环芳烃分布的三维空间插值研究

为准确界定污染场地土壤中多环芳烃在3维条件下的污染分布范围和受污染土方量,选择我国某焦化污染场地苯并(a)芘分布为研究对象,对比研究Krig-3D、IDW-Shepard、IDW-(Franke/Nielson)以及Nearest Neighbor 4种3维插值方法对界定污染范围的不确定性影响。结果表明,不同3维插值模型计算结果差异较大,交叉验证结果显示Krig-3D插值模型插值精度最高,插值结果能较真实地反映场地实际污染情况。通过修复目标对比确定进一步表明,基于4种插值模型计算所得的污染土壤土方量分别为8.51×105、5.62×105、7.12×105、1.09×106m3,选择合理的插值模型将对预测污染范围的不确定性产生重要影响。研究结果对分析污染范围和修复治理过程土方量确定提供重要参考。     

口蹄疫病毒外源序列插入位点的研究进展

伴随着对口蹄疫病毒(FMDV)蛋白结构功能的深入研究,发现FMDV能够表达外源基因片段。通过对FMDV的基因进行改造和修饰研究,进而实现了不同应用目的,如提高病毒滴度、引入标记、提高免疫应答、降低致病性等。文中主要从FMDV接受外源基因插入位点角度来介绍现阶段关于FMDV表达外源基因相关进展。     

The yeast autophagy protease Atg4 is regulated by thioredoxin

Autophagy is a membrane-trafficking process whereby double-membrane vesicles called autophagosomes engulf and deliver intracellular material to the vacuole for degradation. Atg4 is a cysteine protease with an essential function in autophagosome formation. Mounting evidence suggests that reactive oxygen species may play a role in the control of autophagy and could regulate Atg4 activity but the precise mechanisms remain unclear. In this study, we showed that reactive oxygen species activate autophagy in the model yeast Saccharomyces cerevisiae and unraveled the molecular mechanism by which redox balance controls Atg4 activity. A combination of biochemical assays, redox titrations, and site-directed mutagenesis revealed that Atg4 is regulated by oxidoreduction of a single disulfide bond between Cys338 and Cys394. This disulfide has a low redox potential and is very efficiently reduced by thioredoxin, suggesting that this oxidoreductase plays an important role in Atg4 regulation. Accordingly, we found that autophagy activation by rapamycin was more pronounced in a thioredoxin mutant compared with wild-type cells. Moreover, in vivo studies indicated that Cys338 and Cys394 are required for the proper regulation of autophagosome biogenesis, since mutation of these cysteines resulted in increased recruitment of Atg8 to the phagophore assembly site. Thus, we propose that the fine-tuning of Atg4 activity depending on the intracellular redox state may regulate autophagosome formation.