High cell density alters the ratio of type III to I collagen synthesis by fibroblasts

HUMAN fibroblasts in culture synthesise both type I and type III collagen(1), with type I accounting for 70-90% of the total(2). In culture, the rates at which these proteins are synthesised is constant and apparently rather rigidly controlled(3). However, the proportions of these collagens differs in cells cultured with increased amounts of serum (increased type III/I)(4) as well as in cells obtained from patients with certain diseases. Cells from patients with the Ehlers-Danlos type IV syndrome make little or no type III collagen(5,6), whereas cells from patients with osteogenesis imperfecta have an increased type III/I (refs 7, 8). We have found that cells from some patients with systemic sclerosis (scleroderma), have a reduced type III/I ratio. However, as previously reported, these cells grew to a lower density than control cells(9). We report here that normal fibroblasts from human and guinea pig skin produce proportionally more type III collagen at high cell density, probably because of a reduction in the synthesis of type I collagen.     

汞对土壤脲酶的抑制动力学研究

采用实验室模拟的方法研究了重金属汞对2个草甸棕壤和2个黑土脲酶特征参数的影响.结果表明,同一类型土壤,有机质含量与脲酶特征参数之间关系密切Hg明显抑制脲酶活性,二者之间呈显著(P<0.05)或极显著(P<0.01)对数负相关关系,根据相应方程计算得到4个供试土样生态剂量(ED50)值分别为45.75、5.41、10.81和12.41mg/kg.随Hg浓度增加,脲酶动力学参数Km、Vmax和Vmax/Km均减小,除个别处理外,Hg浓度与3参数之间均达到显著或极显著负相关,揭示出脲酶特征参数可从不同角度表征汞对土壤脲酶活性的影响,作用类型表现为典型的反竞争性抑制现象.     

基于密度峰值聚类的高斯混合模型核电运行工况划分

核电厂运行数据记录了核电厂的运行状态,对核电数据进行处理分析从而完成准确的工况划分是实现核电厂运行状态监测的重要基础。为提高核电厂的运行工况划分准确性,本文提出了基于密度峰值聚类的高斯混合模型对核电厂的运行工况进行划分。首先,采用PCA（主成分分析）算法进行数据降维,然后利用密度峰值聚类算法中的决策图确定工况个数,最后利用高斯混合模型完成工况划分。基于真实的核电厂运行数据开展工况划分实验。实验结果表明,本文提出的方法能合理有效地划分出核电运行工况,其三类工况的划分准确率分别达到了99.29%、100%、97.57%,且错误率仅为1.25%。     

抑制荧光法测定阿魏酸钠含量

基于阿魏酸钠对血红蛋白催化H2O2氧化L-酪氨酸的抑制作用提出抑制荧光法测定阿魏酸钠的含量,讨论了测定阿魏酸钠的最佳条件.结果表明:在优化的条件下,阿魏酸钠浓度在6.00×10-8～1.60×10-6 mol·L-1范围内呈良好的线性关系,方法的检出限为1.80×10-8 mol·L-1.此方法用于阿魏酸钠片剂中阿魏酸钠含量的分析,获得满意结果.     

Apoptotic cell death induced by c-myc is inhibited by bcl-2.

Apoptosis is a form of physiological cell death, characterized by chromatin condensation, cytoplasmic blebbing and DNA fragmentation, which often depends on RNA and protein synthesis by the dying cell. The c-myc proto-oncogene, usually implicated in cell transformation, differentiation and cell-cycle progression also has a central role in some forms of apoptosis. These opposing roles of myc in cell growth and death require that other gene products dictate the outcome of c-Myc expression on a cell. A candidate for such a modifying gene is bcl-2, whose product prolongs cell survival and blocks apoptosis in some systems. Here we demonstrate that Bcl-2 prevents apoptotic death induced by c-Myc, provide a mechanism whereby cells can express c-Myc without undergoing apoptosis, and give a possible explanation for the ability of Bcl-2 to synergize with c-Myc in cell transformation.     

Three-dimensional structure of the myosin V inhibited state by cryoelectron tomography

Unconventional myosin V (myoV) is an actin-based molecular motor that has a key function in organelle and mRNA transport, as well as in membrane trafficking. MyoV was the first member of the myosin superfamily shown to be processive, meaning that a single motor protein can 'walk' hand-over-hand along an actin filament for many steps before detaching. Full-length myoV has a low actin-activated MgATPase activity at low [Ca2+], whereas expressed constructs lacking the cargo-binding domain have a high activity regardless of [Ca2+] (refs 5-7). Hydrodynamic data and electron micrographs indicate that the active state is extended, whereas the inactive state is compact. Here we show the first three-dimensional structure of the myoV inactive state. Each myoV molecule consists of two heads that contain an amino-terminal motor domain followed by a lever arm that binds six calmodulins. The heads are followed by a coiled-coil dimerization domain (S2) and a carboxy-terminal globular cargo-binding domain. In the inactive structure, bending of myoV at the head-S2 junction places the cargo-binding domain near the motor domain's ATP-binding pocket, indicating that ATPase inhibition might occur through decreased rates of nucleotide exchange. The actin-binding interfaces are unobstructed, and the lever arm is oriented in a position typical of strong actin-binding states. This structure indicates that motor recycling after cargo delivery might occur through transport on actively treadmilling actin filaments rather than by diffusion.