基于“三带”理论的沉陷区边坡失稳过程分析

地下开采扰动给沉陷区内边坡稳定性带来不利影响。以抚顺老虎台矿开采沉陷区内某边坡失稳破坏为例，分析沉陷区内边坡失稳的动态演化过程。根据开采沉陷学“三带”理论，将处于开采沉陷区的东露天边坡岩土体划分为冒落带、裂隙带、弯曲下沉带和原生带4个特征区域,并分别计算出边坡处于3种“临界状态”时对应的地下开采深度。     

体外消化/Caco-2细胞模型分析发酵对面粉铁生物利用率的影响

中国居民膳食以谷物为主食,谷物中铁吸收率低是造成营养性贫血的主要原因,适当的加工方式可缓解谷物中植酸、多酚等物质对铁生物利用率(Fe bioavailability,FeBV)的影响。为考察酵母发酵对面粉FeBV的影响,采用体外消化/Caco-2细胞模型。结果表明,面团在发酵后pH值呈下降趋势,酸度呈上升趋势;多酚、植酸含量降低,植酸酶活性升高,以上各指标在发酵前后差异均具有统计学意义(P0.05)。发酵后面粉样品的FeBV增加约5%~38%,大多数面粉FeBV发酵前后比较,差异具有统计学意义(P0.05)。结论:发酵可降低面粉的pH值,增加酸度,有利于面粉多酚和植酸的降解以及植酸酶活力的升高,可有效提高面粉FeBV。     

色谱法测定多种农药残留的基质效应研究进展

由于农药残留分析标准化程度的不断深入,基质效应问题越来越受到人们的重视。文章阐述了色谱法中基质效应的涵义、形成机制及影响因素,重点综述了近几年国内外基质效应的消除和补偿方法,包括优化样品前处理方法、采用基质配标法、选择合适的色谱条件、优化质谱分析条件、使用合适同位素内标、分析保护剂法等。基质效应在色谱分析中是客观存在的,使用这些方法,只能有效降低基质效应的影响,但不能完全消除其影响。     

大跨度屋面钢桁架结构吊装地面免加固技术

铁路南昌西站屋面钢桁架存在着单体面积大、结构复杂、工期紧等诸多特点,通过对屋面钢桁架结构型式的研究,并结合地铁、出租车通道、站房主体预应力混凝土框架结构的特点,创造性地提出了主体预留、充分利用出租车通道和地铁隧道箱涵本身刚度,使地面免加固即可行走大吨位履带吊,以南北分向转场吊装屋面钢结构的施工新方法,不仅极大地降低了施工成本,并且安全快速地确保了屋面钢桁架的吊装进度和质量.     

A review of CO2 sorbents for promoting hydrogen production in the sorption-enhanced steam reforming process

Sorption-enhanced-steam-reforming (SESR) is a thermochemical conversion technology that produces a high-purity hydrogen stream by utilizing in-situ removal of CO₂ with a sorbent. In this paper, the advantages and disadvantages of CaO based sorbents, alkali-metal based sorbents (Na₂ZrO₃, Li₂ZrO₃ and Li₄SiO₄), hydrotalcite based sorbents, bifunctional materials and sorbents prepared from wastes are briefly discussed, and the techniques to improve the sorption properties of these CO₂ sorbents are summarized. In the process of hydrogen production by sorption-enhanced-steam-reforming, the selection of suitable high-temperature CO₂ sorbent is the key to produce high purity hydrogen. Furthermore, the hydrogen-production performance of the above-mentioned sorbents in the SESR process is investigated and summarized. Finally, a future perspective and some suggestions regarding these five types of sorbents are put forward.     

CHIR99021 Augmented the Function of Late Endothelial Progenitor Cells by Preventing Replicative Senescence

Endothelial progenitor cells (EPCs) are specialized cells in circulating blood, well known for their ability to form new vascular structures. Aging and various ailments such as diabetes, atherosclerosis and cardiovascular disease make EPCs vulnerable to decreasing in number, which affects their migration, proliferation and angiogenesis. Myocardial ischemia is also linked to a reduced number of EPCs and their endothelial functional role, which hinders proper blood circulation to the myocardium. The current study shows that an aminopyrimidine derivative compound (CHIR99021) induces the inhibition of GSK-3β in cultured late EPCs. GSK-3β inhibition subsequently inhibits mTOR by blocking the phosphorylation of TSC2 and lysosomal localization of mTOR. Furthermore, suppression of GSK-3β activity considerably increased lysosomal activation and autophagy. The activation of lysosomes and autophagy by GSK-3β inhibition not only prevented replicative senescence of the late EPCs but also directed their migration, proliferation and angiogenesis. To conclude, our results demonstrate that lysosome activation and autophagy play a crucial role in blocking the replicative senescence of EPCs and in increasing their endothelial function. Thus, the findings provide an insight towards the treatment of ischemia-associated cardiovascular diseases based on the role of late EPCs.     

ROS-Mediated Anti-Tumor Effect of Coptidis Rhizoma against Human Hepatocellular Carcinoma Hep3B Cells and Xenografts

Coptidis Rhizoma is the dried rhizome from the Coptis chinensis Franch. that has been shown to have a number of beneficial pharmacological properties including antioxidant, anti-inflammatory, and anti-cancer effects. However, the anti-cancer effects of Coptidis Rhizoma on hepatocellular carcinoma (HCC) remain unclear. In this study, we investigated the anti-cancer properties of Coptidis Rhizoma ethanol extract (CR) in HCC Hep3B cells and in a xenograft mouse model. Our results showed that the CR significantly inhibited cell growth and induced apoptosis in Hep3B cells through increased expression of Bcl-2 associated x-protein (Bax) and cleavage of poly-ADP ribose polymerase (PARP), reduced expression of Bcl-2, and activated caspases. CR also increased the generation of intracellular reactive oxygen species (ROS), which caused a loss of mitochondrial membrane potential (MMP, ΔΨm) and activation of the mitochondria-mediated intrinsic apoptosis pathway. Moreover, N-acetylcysteine (NAC), a ROS inhibitor, markedly blocked the effects of CR on apoptotic pathways. CR also induced the expression of light chain 3 (LC3)-I/II, a key autophagy regulator, whereas CR-mediated autophagy was significantly suppressed by NAC. In addition, pre-treatment with NAC perfectly attenuated the inhibition of cell invasion and migration of CR-stimulated Hep3B cells. Furthermore, oral administration of CR suppressed Hep3B tumor growth in xenograft mice without toxicity, alterations to body weight, or changes in hematological and biochemical profiles. Taken together, our findings suggest that CR has anti-tumor effects that result from ROS generation, and may be a potential pharmacological intervention for HCC.