机械设计中的模糊规划模型及其解法

本文应用 Fuzzy 集理论,描述了机械设计中的模糊现象。提出了机械设计的 Fuzzy 最优化方法。并进一步论证了 Fuzzy 最优化可转化为普通规划问题。通过实例计算,证明了本文提出的方法是有效的。     

Edaphic factors determining variation of two ecotypes of Leymus chinensis in North China

Leymus chinensis(Trin.) Tzvel .is a type ofperennial ,rhizome grass with biological andecologicalproperties of resisting drought , poor-nutrient andsalt-alkaline stress .L. chiensiscan adapt to manycomplicated habitats due toits highecological plastici-ty.L. chinensisis always distributed as scatteredpatches with either grey-green or yellow-greenleaves. Steppe dominated by this species is widelydistributed at the eastern end of the Eurasian steppezone. Its main locations in China are the Son…     

镍磷合金镀层的强化性能与机制

本文借助于DSC热扫描仪、电子显微镜和硬度计等仪器,研究了化学沉积镍磷合金镀层的强化性能和机制。试验结果表明,随着镀层的磷含量增加,镀层硬度上升,然后下降;在热处理过程中,镀层的硬度变化经历了一个最大值过程,最高硬度出现在400℃。低磷镀层表现为沉淀强化过程,高磷镀层产生分散强化作用。     

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。     

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.

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

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.     

ICOS is essential for effective T-helper-cell responses

The outcome of T-cell responses after T-cell encounter with specific antigens is modulated by co-stimulatory signals, which are required for both lymphocyte activation and development of adaptive immunity. ICOS, an inducible co-stimulator with homology to CD28, is expressed on activated, but not resting T cells, and shows T-cell co-stimulatory function in vitro. ICOS binds specifically to its counter-receptor B7RP-1 (refs 5,6,7), but not to B7-1 or B7-2. Here we provide in vivo genetic evidence that ICOS delivers a co-stimulatory signal that is essential both for efficient interaction between T and B cells and for normal antibody responses to T-cell-dependent antigens. To determine the physiological function of ICOS, we generated and characterized gene-targeted ICOS-deficient mice. In vivo, a lack of ICOS results in severely deficient T-cell-dependent B-cell responses. Germinal centre formation is impaired and immunoglobulin class switching, including production of allergy-mediating IgE, is defective. ICOS-deficient T cells primed in in vivo and restimulated in vitro with specific antigen produce only low levels of interleukin-4, but remain fully competent to produce interferon-gamma.