天津加快用高新技术改造传统产业的必要性和政策选择

<中共天津市委关于制定天津市国民经济和社会发展第十个五年计划的建议>指出:天津经济社会发展将进入一个新的历史时期,是各项工作全面上水平,实现跨越式发展的重要时期.     

[bmim]Zn_2Cl_5/NH_3溶液的比热容和过量焓

测定了离子液体[bmim]Zn_2Cl_5在T=(323.15~1 173.15)K范围内的热重曲线,结果显示[bmim]Zn_2Cl_5在T637.15 K时具有很高的热稳定性。通过DSC测试得到[bmim]Zn_2Cl_5的比热容数据,在T=(251.15~383.15)K范围内可以用一个圆锥曲线很好地拟合。实验测定了[bmim]Zn_2Cl_5(2)+NH3(1)二元体系溶液的摩尔过量焓,其中氨的摩尔分数x1=(0.60~0.95),温度值为T=288.15 K,303.15 K,318.15 K,333.15 K。采用NRTL模型对过量焓数据进行拟合,得出二元可调参数和非随机参数。过量焓数据的测量误差和最大拟合偏差分别小于4.8%和4.3%。在[bmim]Zn_2Cl_5比热容和[bmim]Zn_2Cl_5/NH3过量焓数据的基础上,计算了氨质量分数w1=(0~1)、温度范围T=(273.15~343.15)K条件下[bmim]Zn_2Cl_5/NH3溶液的焓,所得焓浓图对于研究[bmim]Zn_2Cl_5/NH3吸收式制冷系统性能至关重要。     

14-3-3sigma controls mitotic translation to facilitate cytokinesis

14-3-3 proteins are crucial in a wide variety of cellular responses including cell cycle progression, DNA damage checkpoints and apoptosis. One particular 14-3-3 isoform, sigma, is a p53-responsive gene, the function of which is frequently lost in human tumours, including breast and prostate cancers as a result of either hypermethylation of the 14-3-3sigma promoter or induction of an oestrogen-responsive ubiquitin ligase that specifically targets 14-3-3sigma for proteasomal degradation. Loss of 14-3-3sigma protein occurs not only within the tumours themselves but also in the surrounding pre-dysplastic tissue (so-called field cancerization), indicating that 14-3-3sigma might have an important tumour suppressor function that becomes lost early in the process of tumour evolution. The molecular basis for the tumour suppressor function of 14-3-3sigma is unknown. Here we report a previously unknown function for 14-3-3sigma as a regulator of mitotic translation through its direct mitosis-specific binding to a variety of translation/initiation factors, including eukaryotic initiation factor 4B in a stoichiometric manner. Cells lacking 14-3-3sigma, in marked contrast to normal cells, cannot suppress cap-dependent translation and do not stimulate cap-independent translation during and immediately after mitosis. This defective switch in the mechanism of translation results in reduced mitotic-specific expression of the endogenous internal ribosomal entry site (IRES)-dependent form of the cyclin-dependent kinase Cdk11 (p58 PITSLRE), leading to impaired cytokinesis, loss of Polo-like kinase-1 at the midbody, and the accumulation of binucleate cells. The aberrant mitotic phenotype of 14-3-3sigma-depleted cells can be rescued by forced expression of p58 PITSLRE or by extinguishing cap-dependent translation and increasing cap-independent translation during mitosis by using rapamycin. Our findings show how aberrant mitotic translation in the absence of 14-3-3sigma impairs mitotic exit to generate binucleate cells and provides a potential explanation of how 14-3-3sigma-deficient cells may progress on the path to aneuploidy and tumorigenesis.     

Natural polymorphisms in C. elegans HECW-1 E3 ligase affect pathogen avoidance behaviour

Heritable variation in behavioural traits generally has a complex genetic basis, and thus naturally occurring polymorphisms that influence behaviour have been defined only in rare instances. The isolation of wild strains of Caenorhabditis elegans has facilitated the study of natural genetic variation in this species and provided insights into its diverse microbial ecology. C. elegans responds to bacterial infection with conserved innate immune responses and, although lacking the immunological memory of vertebrate adaptive immunity, shows an aversive learning response to pathogenic bacteria. Here, we report the molecular characterization of naturally occurring coding polymorphisms in a C. elegans gene encoding a conserved HECT domain-containing E3 ubiquitin ligase, HECW-1. We show that two distinct polymorphisms in neighbouring residues of HECW-1 each affect C. elegans behavioural avoidance of a lawn of Pseudomonas aeruginosa. Neuron-specific rescue and ablation experiments and genetic interaction analysis indicate that HECW-1 functions in a pair of sensory neurons to inhibit P. aeruginosa lawn avoidance behaviour through inhibition of the neuropeptide receptor NPR-1 (ref. 10), which we have previously shown promotes P. aeruginosa lawn avoidance behaviour. Our data establish a molecular basis for natural variation in a C. elegans behaviour that may undergo adaptive changes in response to microbial pathogens.     

我校与陕西福天宝集团公司签定技术转让协议

20 0 0年 1 1月 9日 ,我校与陕西福天宝集团公司在该集团公司举行了“年产 50 0 t含重金属离子污水处理剂 DTCR技术成果转让签约仪式”,技术转让费成交 60万元。这是继 7日在杨凌农高会对该项目拍卖后双方具有实质性进展的再合作。我校副校长朱恪孝 ,“2 1 1工程”办公室、科研处有关负责人 ,以及陕西福天宝集团公司董事长吴言强、总经理黄翠萍等出席了签约仪式。这项技术成果是由我校化学研究所孙来九教授、王文丰副教授等人开发研制的环保产品 ,该产品是一种液体高分子螯合树脂 ,能与废水中的重金属离子迅速反应生成水不溶性络合盐而达…     

粉煤灰/壳聚糖复合材料处理高浊水的研究

为解决高浊水除浊问题，使用酸改性粉煤灰与壳聚糖按照不同质量比制备成的复合材料对高浊水进行处理。通过单因素实验和正交试验得出了粉煤灰与壳聚糖复合材料投加量、搅拌时间、pH和废水初始浊度对除浊性能的影响以及各因素综合作用对除浊率的影响。单因素实验结果表明：当粉煤灰与壳聚糖质量比为6:1时，其除浊率可达到93.78%；当复合材料CWF3投加量为0.6 g时，其除浊率可达到73.52%；当搅拌时间为30 min时，其除浊率可达到90.28%；当pH=6时，其除浊率可达到84.50%；当初始浊度为300 NTU时，其除浊率可达到95.67%。正交试验结果表明，当粉煤灰与壳聚糖质量比为6:1，最佳组合条件为投加量0.7 g、搅拌时间35 min、废水初始pH=7、废水初始浊度350 NTU。酸改性粉煤灰负载壳聚糖后具有更强的亲和能力，且价格便宜，可以弥补单独使用粉煤灰或壳聚糖的不足，可用于对大规模废水进行处理。     

人偶（下）

就这么走进大厦？当然不行，这地方是属于私人的。私人企业，一般就意味着麻烦的根源，现在想要进入同样也是一个大麻烦。     

基于DMSP/OLS数据的全国空气污染物时空演变研究

基于美国国防气象卫星搭载传感器DMSP/OLS的夜间灯光遥感影像，从2000—2013年选取4年进行影像采集、影像校正等操作后，提取了灯光总量、灯光面积数据，根据年份间夜间灯光数据的增长量开展了全国各区域间的差异分析，结合空气污染物排放量进行了相关度分析。研究结果发现：（1）整体上全国夜间灯光量增幅变大，且增幅受相关年份政策影响。（2）夜间灯光总量与空气污染物排放量呈现正相关性，且两者相关系数较高；工业空气污染物与夜间灯光量相关性不断降低，同时生活空气污染物与夜间灯光量相关性不断提高。（3）夜间灯光总量与空气污染的高/高集聚区域一致性稳步提升。结合夜间灯光影像数据与空气污染数据，通过比较夜间灯光数据差异探讨空气污染物的时空演变，为我国空气污染的综合治理提供了一个新的视角。     

基于网络药理学研究厚朴-杏仁治疗哮喘的潜在作用机制

本研究采用网络药理学方法分析厚朴-杏仁配伍治疗哮喘的潜在作用机制。通过BATMAN-TCM数据库检索厚朴、杏仁的中药化学成分及靶标信息，PALM-IST数据库搜索疾病靶标信息，string数据库构建靶标的蛋白质相互作用网络，利用Cytoscape v3.5.1对药物靶标相互作用进行可视化分析，DAVID数据库和Cytoscape v3.5.1的ClueGO+CluePedia插件对药物关键靶标进行GO生物功能富集分析和KEGG信号通路富集分析。共检索到厚朴-杏仁化合物51个，靶标435个，哮喘疾病相关靶标415个，进而分析得到药物治疗疾病关键靶标14个，包括肿瘤坏死因子、过氧化氢酶、白介素13、β2肾上腺素能受体等；GO基因功能分析主要涉及应激反应调控、先天性免疫反应调控、防御反应、急性炎症反应、刺激反应、凝血止血调节、自我内稳定、活性氧代谢过程等生物过程；KEGG分析主要参与NF-κB、IL-17、FcεRI、Toll受体及FoxO等信号通路。厚朴-杏仁能通过多个靶点、多种途径、多条通路对哮喘的气道慢性炎症、气道重塑和气道高反应起潜在治疗作用。     

Calcium-induced cleavage of DNA topoisomerase I involves the cytoplasmic-nuclear shuttling of calpain 2

Important to the function of calpains is temporal and spatial regulation of their proteolytic activity. Here, we demonstrate that cytoplasm-resident calpain 2 cleaves human nuclear topoisomerase I (hTOP1) via Ca²⁺-activated proteolysis and nucleoplasmic shuttling of proteases. This proteolysis of hTOP1 was induced by either ionomycin-caused Ca²⁺ influx or addition of Ca²⁺ in cellular extracts. Ca²⁺ failed to induce hTOP1 proteolysis in calpain 2-knockdown cells. Moreover, calpain 2 cleaved hTOP1 in vitro. Furthermore, calpain 2 entered the nucleus upon Ca²⁺ influx, and calpastatin interfered with this process. Calpain 2 cleavage sites were mapped at K¹⁵⁸ and K¹⁸³ of hTOP1. Calpain 2-truncated hTOP1 exhibited greater relaxation activity but remained able to interact with nucleolin and to form cleavable complexes. Interestingly, calpain 2 appears to be involved in ionomycin-induced protection from camptothecin-induced cytotoxicity. Thus, our data suggest that nucleocytoplasmic shuttling may serve as a novel type of regulation for calpain 2-mediated nuclear proteolysis.