含镍磁黄铁矿硝酸浸出液中硝酸镁与硫酸镁的分离

硝酸催化浸出是处理金属硫化物的有效方法。用这种方法在较低温度和氧压下成功地处理了含镍磁黄铁,但矿石中的氧化镁与硫酸和硝酸反应生成硫酸镁和硝酸镁,后者消耗了大量硝酸;因而需要分离硫酸镁,返回使用硝酸镁才能保证浸出过程经济地进行。本研究测定了Mg(NO_3)_2-MgSO_4-H_2O系在343K,308K,以及Mg(NO_3)_2-MgSO_4-C_2H_5OH-H_2O系在298K的平衡相图。结果表明,蒸发结晶法及乙醇结晶法均能有效地分离出硫酸镁,但后者更为节能。加10％乙醇即可使硫酸镁与硝酸镁较好分离。     

以分析法比较流体的换热性能

基于换热过程中的损失率能定量地反映该过程中流体的传热与流动的综合性能这一特性，借助换热过程的损失率方程，分析比较了几种流体工质在不同换热方式下的综合特性。比较结果表明，液体（如水）有远优于气体（如空气）的流动与传热的综合性能，且随着流体温度的升高其优势更为明显。同时表明分析法在定量评价换热工质性能的突出特点及工程上的应用价值。     

Angiotensin-converting enzyme 2 is an essential regulator of heart function

Cardiovascular diseases are predicted to be the most common cause of death worldwide by 2020. Here we show that angiotensin-converting enzyme 2 (ace2) maps to a defined quantitative trait locus (QTL) on the X chromosome in three different rat models of hypertension. In all hypertensive rat strains, ACE2 messenger RNA and protein expression were markedly reduced, suggesting that ace2 is a candidate gene for this QTL. Targeted disruption of ACE2 in mice results in a severe cardiac contractility defect, increased angiotensin II levels, and upregulation of hypoxia-induced genes in the heart. Genetic ablation of ACE on an ACE2 mutant background completely rescues the cardiac phenotype. But disruption of ACER, a Drosophila ACE2 homologue, results in a severe defect of heart morphogenesis. These genetic data for ACE2 show that it is an essential regulator of heart function in vivo.     

ELNF归约演算

ＥＬＮＦ演算是在ＬＮＦ演算的基础上扩充而成的函数／逻辑归约演算系统，扩充的主要工作包括逻辑变量、谓词名的引进。提出并描述了逻辑函子ＳＯＬＵＴＩＯＮ和ＰＲＯＶＥ及其归约规则．讨论了ＥＬＮＦ演算的基本概念。为表征ＨＯＲＮ子句提供了一种有效方式。     

MRT-2 checkpoint protein is required for germline immortality and telomere replication in C. elegans

The germ line is an immortal cell lineage that is passed indefinitely from one generation to the next. To identify the genes that are required for germline immortality, we isolated Caenorhabditis elegans mutants with mortal germ lines--worms that can reproduce for several healthy generations but eventually become sterile. One of these mortal germline (mrt) mutants, mrt-2, exhibits progressive telomere shortening and accumulates end-to-end chromosome fusions in later generations, indicating that the MRT-2 protein is required for telomere replication. In addition, the germ line of mrt-2 is hypersensitive to X-rays and to transposon activity. Therefore, mrt-2 has defects in responding both to damaged DNA and to normal double-strand breaks present at telomeres. mrt-2 encodes a homologue of a checkpoint gene that is required to sense DNA damage in yeast. These results indicate that telomeres may be identified as a type of DNA damage and then repaired by the telomere-replication enzyme telomerase.     

Preparation of composite tubular grafts for vascular repair via electrospinning

A novel type of composite vascular graft was developed via electrospinning in the present investigation.Collagen and chitosan were blended to form the inner and outer layer.Poly(1-lactide-co-caprolacto...     

RNAi-mediated gene silencing in non-human primates

The opportunity to harness the RNA interference (RNAi) pathway to silence disease-causing genes holds great promise for the development of therapeutics directed against targets that are otherwise not addressable with current medicines. Although there are numerous examples of in vivo silencing of target genes after local delivery of small interfering RNAs (siRNAs), there remain only a few reports of RNAi-mediated silencing in response to systemic delivery of siRNA, and there are no reports of systemic efficacy in non-rodent species. Here we show that siRNAs, when delivered systemically in a liposomal formulation, can silence the disease target apolipoprotein B (ApoB) in non-human primates. APOB-specific siRNAs were encapsulated in stable nucleic acid lipid particles (SNALP) and administered by intravenous injection to cynomolgus monkeys at doses of 1 or 2.5 mg kg(-1). A single siRNA injection resulted in dose-dependent silencing of APOB messenger RNA expression in the liver 48 h after administration, with maximal silencing of >90%. This silencing effect occurred as a result of APOB mRNA cleavage at precisely the site predicted for the RNAi mechanism. Significant reductions in ApoB protein, serum cholesterol and low-density lipoprotein levels were observed as early as 24 h after treatment and lasted for 11 days at the highest siRNA dose, thus demonstrating an immediate, potent and lasting biological effect of siRNA treatment. Our findings show clinically relevant RNAi-mediated gene silencing in non-human primates, supporting RNAi therapeutics as a potential new class of drugs.     

Dynamic Analysis of Cable Roofs Under Transient Wind:A Comparison Between Time Domain and Frequency Domain Approaches

At present, high-speed computing capabilities and advanced nonlinear dynamic finite element procedures enable detailed dynamic analysis of cable structures. Although deterministic approaches require considerable analysis time and effort in relation to modeling, running, and data processing, they seem to be the only alternative to obtain high accuracy. Detailed dynamic analysis of cable roof networks is sophisticated and requires advanced modeling expertise. This paper presents a comparison between detailed nonlinear dynamic analysis and a simplified frequency domain approach to estimate the maximum probable response of weakly nonlinear cable roofs. The approach can be considered as alternative to detailed time-domain analysis in the preliminary design phase, or can be used to validate results obtained from more elaborated numerical models. The proposed method is illustrated with two examples of cable net roofs that were also analysed in the time domain.     

嵌套式建模支持

阐述了人的建模思维机制。引入等价关系和划分作为问题粒度研究的基础，定义了逆商集，使之与商集一起，构成了对问题不同粒度的完整描述，并讨论了粒度的性质，借助拓扑分析，给出了问题可分解、可细化和粗化、细化等一系列定义，在问题簇和模型簇概念的基础上，提出了嵌套式建模（支持）作为面向复杂系统的建模支持方法论，具体给出了其实施步骤，这是一个人机交互的启发式过程，将嵌套式建模与传统式建模作了比较，此外还作了若干说明。     

Inactivation of the apoptosis effector Apaf-1 in malignant melanoma

Metastatic melanoma is a deadly cancer that fails to respond to conventional chemotherapy and is poorly understood at the molecular level. p53 mutations often occur in aggressive and chemoresistant cancers but are rarely observed in melanoma. Here we show that metastatic melanomas often lose Apaf-1, a cell-death effector that acts with cytochrome c and caspase-9 to mediate p53-dependent apoptosis. Loss of Apaf-1 expression is accompanied by allelic loss in metastatic melanomas, but can be recovered in melanoma cell lines by treatment with the methylation inhibitor 5-aza-2'-deoxycytidine (5aza2dC). Apaf-1-negative melanomas are invariably chemoresistant and are unable to execute a typical apoptotic programme in response to p53 activation. Restoring physiological levels of Apaf-1 through gene transfer or 5aza2dC treatment markedly enhances chemosensitivity and rescues the apoptotic defects associated with Apaf-1 loss. We conclude that Apaf-1 is inactivated in metastatic melanomas, which leads to defects in the execution of apoptotic cell death. Apaf-1 loss may contribute to the low frequency of p53 mutations observed in this highly chemoresistant tumour type.