润滑脂及其添加剂剖析

本文主要介绍采用柱层析分离与红外光谱配合,对从美国进口的特种润滑脂进行剖析,使用渗析法将润滑脂中基础油抽提出,用柱色谱分离出润滑脂中抗氧剂等四种添加剂,并由红外光谱图获得其相应的结构范围,柱色谱洗脱剂通过寻找薄层包谱展开剂来选择,洗出液用薄层层析跟踪,按跟踪薄层结果,将柱层析收集相同的纯组分合并驱除溶剂作红外光谱分析。     

矿物和岩石的魔幻世界

这是一本图册集，收录了欧洲、美国、澳大利亚和冰岛等国的135张精美的彩色照片，从辽阔的岩石风景照片，到微小的细节特写，范围跨度极大。图册中水晶、宝石和化石的特写镜头与岩石和矿物的薄而透明的细微纹理图案的微缩图像交替出现。作者或如实记录或添加修饰地“放大”了主题，带领读者走进各种各样令人惊讶的新形态和透视的空间，时而抽象，时而现实。     

A Fingerprinting Method Based on Module Extraction Used to Protect Intellectual Property

Intellectual Property （IP） reuse methodology has been widely used in Integrate Circuit （IC） design. Meanwhile, the corresponding security problems caused by illegal IP distribution have aroused lots of attentions. Unlike using IP watermark to identify IP＇s ownership, IP fingerprinting can be used to trace illegal distributor. In this paper, IP buyer＇s fingerprint is mapped into different derived instances of extracted modules, and then is embedded into IP to identify distributor in case of illegal distribution. Comparing with other fingerprinting method, the proposed method has some good characteristics such as low design effort, small storage demand, high security and few physical overheads.     

Improved method of large scale purification of acetylcholinesterase from the electric eel (Electrophorus electricus) by affinity chromatography

Résumé Une méthode basée sur d'affinité chromatographique nous a permis de purifier complètement l'acétylcholinestérase des organes électriques du gymnote (Electrophorus electricus). L'activité spécifique de l'acétylcholinestérase ainsi établie en milligrammes dépasse 950 mM de substrat hydrolysé (acétylcholine)/mg protéine/h et sa pureté a été vérifiée par électrophorèse sur gel de polyacrylamide.

---

---

This work was supported by grants: USPHS No. GM-01839 and U.C. San Francisco Academic Senate Research Committee, Grant No. 46.     

Iron corrosion by novel anaerobic microorganisms

Corrosion of iron presents a serious economic problem. Whereas aerobic corrosion is a chemical process, anaerobic corrosion is frequently linked to the activity of sulphate-reducing bacteria (SRB). SRB are supposed to act upon iron primarily by produced hydrogen sulphide as a corrosive agent and by consumption of 'cathodic hydrogen' formed on iron in contact with water. Among SRB, Desulfovibrio species--with their capacity to consume hydrogen effectively--are conventionally regarded as the main culprits of anaerobic corrosion; however, the underlying mechanisms are complex and insufficiently understood. Here we describe novel marine, corrosive types of SRB obtained via an isolation approach with metallic iron as the only electron donor. In particular, a Desulfobacterium-like isolate reduced sulphate with metallic iron much faster than conventional hydrogen-scavenging Desulfovibrio species, suggesting that the novel surface-attached cell type obtained electrons from metallic iron in a more direct manner than via free hydrogen. Similarly, a newly isolated Methanobacterium-like archaeon produced methane with iron faster than do known hydrogen-using methanogens, again suggesting a more direct access to electrons from iron than via hydrogen consumption.     

HAb18G/CD147-mediated calcium mobilization and hepatoma metastasis require both C-terminal and N-terminal domains

HAb18G/CD147 is a heavily glycosylated protein containing two immunoglobulin superfamily domains. Our previous studies have indicated that overexpression of HAb18G/CD147 enhances metastatic potentials in human hepatoma cells by disrupting the regulation of store-operated Ca²⁺ entry by nitric oxide (NO)/cGMP. In the present study, we investigated the structure-function of HAb18G/CD147 by transfecting truncated HAb18G/CD147 fragments into human 7721 hepatoma cells. The inhibitory effect of HAb18G/CD147 on 8-bromo-cGMP-regulated thapsigargin-induced Ca²⁺ entry was reversed by the expression of either C or N terminus truncated HAb18G/CD147 in T7721C and T7721N cells, respectively. The potential effect of HAb18G/CD147 on metastatic potentials, both adhesion and invasion capacities, of hepatoma cells was abolished in T7721C cells, but not affected in T7721N cells. Release and activation of matrix metalloproteinases (MMPs), MMP-2 and MMP-9, were found to be enhanced by the expression of HAb18G/CD147, and this effect was abolished by both truncations. Thapsigargin significantly enhanced release and activation of MMPs (MMP-2 and MMP-9) in non-transfected 7721 cells, and this effect was negatively regulated by SNAP. However, no effects of thapsigargin or SNAP were observed in T7721 cells, and expression of HAb18G/CD147 enhanced secretion and activation of MMPs at a stable and high level. Taken together, these results suggest that both ectodomain and intracellular domains of HAb18G/CD147 are required to mediate the effect of HAb18G/CD147 on the secretion and activation of MMPs and metastasis-related processes in human hepatoma cells by disrupting the regulation of NO/cGMP-sensitive intracellular Ca²⁺ mobilization although each domain may play different roles.Received 1 April 2004; received after revision 15 June 2004; accepted 22 June 2004     

What’s new in the renin-angiotensin system?

Activation of the type 1 angiotensin II receptor (AT(1)R) is associated with the aetiology of left ventricular hypertrophy, although the exact intracellular signalling mechanism(s) remain unclear. Transactivation of the epidermal growth factor receptor (EGFR) has emerged as a central mechanism by which the G protein-coupled AT(1)R, which lacks intrinsic tyrosine kinase activity, can stimulate the mitogen-activated protein kinase signalling pathways thought to mediate cardiac hypertrophy. Current studies support a model whereby AT(1)R-dependent transactivation of EGFRs on cardiomyocytes involves stimulation of membrane-bound metalloproteases, which in turn cleave EGFR ligands such as heparin-binding EGF from a plasma membrane-associated precursor. Numerous aspects of the 'triple membrane-passing signalling' paradigm of AT(1)R-induced EGFR transactivation remain to be characterised, including the identity of the specific metalloproteases involved, the intracellular mechanism for their activation and the exact EGFR subtypes required. Here we examine how 'hijacking' of the EGFR might explain the ability of the AT(1)R to elicit the temporally and qualitatively diverse responses characteristic of the hypertrophic phenotype, and discuss the ramifications of delineating these pathways for the development of new therapeutic strategies to combat cardiac hypertrophy.