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.     

独立学院本科毕业论文(设计)问卷调查分析

通过对独立学院2012届化学系学生完成毕业论文(设计)期间问卷调查分析得知,72%的是在学校规定的3~4个月完成的,文献查阅的主要途径是在学校图书馆和宿舍,他们完成毕业论文(设计)的场所多样化了,实验室、宿舍、图书馆和实习公司是主要场所,与指导教师交流方式主要有直接见面、QQ聊天和电子邮件.虽然目前各方面都得到很大的改善,但还是有很多因素造成完成毕业论文困难,主要的困难是专业知识不足、实验条件有限、文献资源不足和学生时间分配不合理.     

WNT7b mediates macrophage-induced programmed cell death in patterning of the vasculature

Macrophages have a critical role in inflammatory and immune responses through their ability to recognize and engulf apoptotic cells. Here we show that macrophages initiate a cell-death programme in target cells by activating the canonical WNT pathway. We show in mice that macrophage WNT7b is a short-range paracrine signal required for WNT-pathway responses and programmed cell death in the vascular endothelial cells of the temporary hyaloid vessels of the developing eye. These findings indicate that macrophages can use WNT ligands to influence cell-fate decisions--including cell death--in adjacent cells, and raise the possibility that they do so in many different cellular contexts.     

实验性急性肺损伤部分液体通气效应与剂量的关系

目的:对肺灌洗诱导的急性肺损伤家兔实施不同剂量氟碳(perfluorocarbon,PFC)的部分液体通气(partialliquidventilation,PLV),观察其疗效及剂量-效应关系。方法:14只成年健康家兔,麻醉后经气管导管用生理盐水反复肺内灌洗,直至动脉氧分压(PaO2)<13 33kPa(100mmHg)达1h,记录肺气体交换、血液动力学及呼吸动力各参数作为肺损伤(acutelunginjury,ALI)基础值。随机分为PLV组及对照组,对照组以呼吸机行常规机械通气,不给予任何治疗措施;PLV组动物于ALI后每30min气管内灌入PFC(FC3280,3M,德国)6mL·kg-1共3次,总量为18mL·kg-1。以上述呼吸参数行机械通气。最后一次灌注后继续行机械通气3h,每小时记录各参数次。结果:PLV组PaO2及动脉血氧饱和度(HbO2)在灌注第一个剂量的PFC后即显著改善,并与剂量呈相关性;PaCO2在灌注第一个PFC剂量后较ALI时显著降低,但并不随剂量的增加而继续降低。结论:以氟碳为媒介的部分液体通气可明显改善肺灌洗诱导的急性肺损伤家兔的肺氧合,并呈剂量相关性,同时呼吸动力的改善与剂量无关。     

集成Intserv Diffserv 和MPLS改善IP QoS

讨论了 Intserv,Diffserv和 MPLS集成模型的功能及服务类型之间的映射。在边缘网络使用 RSVP,在核心网络使用 CR- LDP作信令协议进行资源预留或建立交换路径 ,对核心网络中的标记边缘路由器 LER和标记交换路由器 LSR的结构和功能进行了设计和说明     

基于可逆记忆CA融合时间延迟的图像加密算法研究

针对当前的元胞自动机加密系统不具备记忆功能,使其安全性\加密速度不理想;且目前的图像加密算法都忽略考虑时间延迟现象,无法体现加密的真实过程。对此,提出一种可逆线性记忆元胞自动机(cellular automata-CA)与时间延迟函数,采用二者相融合的加密算法来克服上述问题;并将非线性耦合置乱方法引入算法中。首先迭代一维线性分段映射所得到的一维数组,该数组通过非线性耦合置乱方法后得到一个置乱数组,并利用该数组对初始图像进行置乱处理,改变像素位置;然后将时间延迟引入到Logistic映射中,利用可逆线性记忆元胞自动机的演变规则对二者相融合所生成的时间延迟伪随机数组进行迭代,得到迭代数组。利用该迭代数组根据像素扩散机制对置乱图像进行扩散加密处理,改变其像素值。借助MATLAB仿真软件来验证算法。结果表明:提出的图像加密新算法具有优异的加密性能,加密机制高度安全,其密钥空间巨大,抗攻击能力大幅度提升。     

Buyer - seller Relationships in Hong Kong's Clothing Industry

The aim of this study is to examine the buyer-seller re-lationship in Hong Kong's clothing industry.The initialpart investigated the industry's environment.Four hy-pothesis were developed which were based on the long-term buyer-seller relationships'features.The benefitsthat can enjoy within the stage of long-term buyer-seller relationships was the defined and suggested.     

民办高校党组织与董事会关系探究

随着民办高校的发展,民办高校党建工作在逐渐步入正轨的同时面临许多发展难题,其中最核心的是民办高校党组织与董事会的关系问题。从理论来看,二者之间的关系为决策与参与决策、监督与被监督、引导与被引导、分工协作,但在实践中却出现分权不清、失衡、权力运作失范、制度缺失严重、机制运作失调等问题,因此,只有转变观念,准确定位,建立框架科学、细节完备的制度体系,打造良性互动的科学机制,夯实基础、循序渐进才能处理好二者的关系,推进民办高校健康发展。