MPC Applicantion in Alcohol Distillation

针对酒精生产中精馏塔控制的塔顶温度和塔底温度的强耦合性，使用模型预测控制代替常规的PID控制，使用西门子的PCS7系统予以实现，同传统控制相比，在控制效果上有很大的提高

罗布泊湖心区近地表层微量元素分布及其环境意义

罗布泊湖心区近地表层微量元素分布特征为:同类元素的含量变化趋势基本一致,如较稳定元素Ti、Cr、Co、N i,在中部60-250cm层段含量高,但有所波动;活动性中等的Cu、Pb、As其变化则以198cm为界,上段含量少、变幅小;另外还有些元素在上段相应层位中缺失,如Nb在24-48cm和78-150cm段、Zr在36-42cm和78-144cm段缺失。微量元素含量的分段与岩性的变化基本一致。不同时段离子类型、含量以及微量元素的差异在一定程度上反映相应阶段的环境特征

新疆罗布泊西岸地区河湖地貌特征及其成因

罗布泊西岸地区的塔里木河谷地貌带的第一道天然堤形成时间应有数百年,第二道天然堤与一道之间间隔时间较长,但也至少在100-200年以上,三、四道天然堤的形成时间应属近代。小河古湖积平原在2 000 a BP前后,环境有所好转,1 700 a BP前后环境又恶化。罗布沙漠西缘风沙地貌带是近代罗布沙漠不断向西推移,使原先的河湖冲积平原地表被沙丘覆盖形成风沙地貌。罗布泊湖积台地以楼兰故城一带分布最广,地面切割深度一般在6 m左右。孔雀河三角洲前缘的孔雀河末端河道似具有由南向北迁移的特点,第一期古河道可形成于2 000 a BP,第二和第三期古河道应形成于2 000 a BP前后,第四期古河道形成于20世纪20-50年代。河湖地貌过程与罗布泊环境变迁密切相关。近代罗布泊可分东湖和西湖两部分,其间被高3～5 m由北向南延伸的半岛相隔。罗布泊东湖早在3 000 a BP前后就已干涸,罗布泊西湖干涸的时间可能也在20世纪60年代中后期

罗布泊地区红柳沙包纹层沙粒度特征与环境指示意义

通过对罗布泊西南缘一个红柳沙包的132个清晰沉积纹层沙物质特征分析表明:所有沉积纹层沙物质均以细砂为主,占42.54～91.82%,其中1871-1874年纹层砂粒最细,1903-1910年纹层砂粒最粗;沙物质粒径分布在0.044～0.283mm之间,平均值0.095mm,中值粒径0.083mm;所有纹层沙物质的分选性都很好,分选系数分布在0.04～0.06之间,平均值0.05;偏态值分布在0.14～0.35之间,平均值0.19;峰态值分布在1.03～1.17之间,平均值1.13;沙物质粒度分维值分布在1.39～2.88之间,平均值2.80。除沙层厚度外,粒级组成、粒度特征参数、粒级分布曲线以及粒度累计概率曲线等也有较明确的环境指示意义

Aldose reductase regulates miR-200a-3p/141-3p to coordinate Keap1-Nrf2, Tgf beta 1/2, and Zeb1/2 signaling in renal mesangial cells and the renal cortex of diabetic mice

973 Program of China [2009CB941601]; National Science Foundation of China [31271239]; Fujian Provincial Department of Science and Technology [2010L0002]; 111 Project of Education of China [B06018]; Open Research Fund of the State Key Laboratory of Cellular Stress Biology, Xiamen University [SKLCSB2012KF005]; China Postdoctoral Foundation [2012M511446]Aberrant regulation in oxidative stress, fibrogenesis, and the epithelial-mesenchymal transition (EMT) in renal cells under hyperglycemic conditions contributes significantly to the onset and progression of diabetic nephropathy. The mechanisms underlying these hyperglycemia-induced dysregulations, however, have not been dearly elucidated. Herein, we report that aldose reductase is capable of regulating the expression of miR-200a-3p/141-3p negatively in renal mesangial cells. MiR-200a-3p/141-3p, in turn, act to target Keap1, Tgf beta 2, fibronectin, and Zeb2 directly and regulate Tgf beta 1 and Nrf2 indirectly under high-glucose conditions, resulting in profound dysregulations in Keap1-Nrf2, Tgf beta 1/2, and Zeb1/2 signaling. In vivo in streptozotocin-induced diabetic mice, we found that aldose reductase deficiency caused significant elevations in miR-200a-3p/141-3p in the renal cortex, which were accompanied by a significant downregulation of Keap1, Tgf beta 1/2, and fibronectin but significant upregulation of Nrf2. Moreover, in vivo administration of inhibitors of miR-200a-3p in diabetic animals significantly exacerbated cortical and glomerular fibrogenesis and increased urinary albumin excretion, tightly linking dysregulated miR-200a-3p with the development of diabetic nephropathy. Collectively, our results reveal a novel mechanism whereby hyperglycemia induces aldose reductase to regulate renal expression of miR-200a-3p/141-3p to coordinately control hyperglycemia-induced renal oxidative stress, fibrogenesis, and the EMT. Our novel findings also suggest that inhibition of aldose reductase and in vivo renal cortical restoration of miR-200a-3p/141-3p or their combination are very promising avenues for the development of therapeutic strategies or drugs against diabetic nephropathy. (C) 2013 The Authors. Published by Elsevier Inc. All rights reserved