Ex vivo expansion with stem cell factor and interleukin-11 augments both short-term recovery posttransplant and the ability to serially transplant marrow

The characterization of many cytokines involved in the control of hematopoiesis has led to intense investigation into their potential use in ex vivo culture to expand progenitor numbers. We have established the optimum ex vivo culture conditions that allow substantial amplification of transient engrafting murine stem cells and which, simultaneously, augment the ability to sustain serial bone marrow transplantation (BMT). Short-term incubation of unfractionated BM cells in liquid culture with stem cell factor (SCF) and interleukin-11 (IL-11) produced a 50-fold amplification of clonogenic multipotential progenitors (CFU-A). Following such ex vivo expansion, substantially fewer cells were required to rescue lethally irradiated mice. When transplanted in cell doses above threshold for engraftment, BM cells expanded ex vivo resulted in significantly more rapid hematopoietic recovery. In a serial transplantation model, unmanipulated BM was only able to consistently sustain secondary BMT recipients, but BM expanded ex vivo has sustained quaternary BMT recipients that remain alive and well more than 140 days after 4th degree BMT. These results show augmentation of both short-term recovery posttransplant and the ability to serially transplant marrow by preincubation in culture with SCF and IL-11.     

Phase equilibrium in a polarized saturated3He—4He mixture

We present experimental results on the phase equilibrium of a saturated³He−⁴He mixture, which has been cooled to a temperature of 10–15 mK and polarized in a⁴He circulating dilution refrigerator to a stationary polarization of 15%, 7 times higher than the equilibrium polarization in the external field of 7 T. The pressure dependence of the polarization enhancement in the refrigerator shows that the molar susceptibilities of the concentrated and dilute phase of a saturared³He-⁴He mixture are equal atp=2.60±0.04 bar. This result affects the Fermi liquid parameters of the dilute phase. The osmotic pressure in the dilute phase has been measured as a function of the polarization of the coexisting concentrated phase up to 15%. We find that the osmotic pressure at low polarization (<7%) agrees well with thermodynamics using the new Fermi liquid parameters of the dilute phase.     

浅谈EPC总承包工程项目质量管理

结合EPC工程项目管理特点，将质量管理的基本要素充分体现在每一个工作环节，确保工程质量符合规程规范和业主质量目标要求，为机组今后正常稳定运行奠定坚实的基础。     

直流非转移弧等离子喷枪中电弧的工作特性研究

利用计算机数值模拟技术，采用有限容积方法，针对自制的低能耗、高效率内送粉等离子喷涂设备，对喷枪内部电弧长度及其对流体特性的影响进行了分析研究。结果表明，通过增加进气流量和减少电流的大小，均使得等离子电弧长度增加，阳极弧根位置逐渐向下游移动，但是产生这两种现象的机理以及对气流温度和速度的影响是不同的。     

主动式红外光电靶的研究

提出了采用红外光源的主动式光电靶的设计构想，用以消除传统天幕靶在对低速弹测量时，声音对测量的干扰，并设计了整个实验方案，在对静态实验结果进行分析的基础上，证明了该种方法的可行性。     

Insulin-like growth factor I activates the invasion suppressor function of E-cadherin in MCF-7 human mammary carcinoma cells in vitro

The calcium-dependent cell-cell adhesion molecule E-cadherin has been shown to counteract invasion of epithelial neoplastic cells. Using three monoclonal antibodies, we have demonstrated the presence of E-cadherin at the surface of human MCF-7/6 mammary carcinoma cells by indirect immunofluorescence coupled to flow cytometry and by immunocytochemistry. Nevertheless, MCF-7/6 cells failed to aggregate in a medium containing 1.25 mM CaCl2, and they were invasive after confrontation with embryonic chick heart fragments in organ culture. Treatment of MCF-7/6 cells with 0.5 microgram ml-1 insulin-like growth factor I (IGF-I) led to homotypic aggregation within 5 to 10 min and inhibited invasion in vitro during at least 8 days. The effect of IGF-I on cellular aggregation was insensitive to cycloheximide. However, monoclonal antibodies that interfered with the function of either the IGF-I receptor (alpha IR3) or E-cadherin (HECD-1, MB2) blocked the effect of IGF-I on aggregation. The effects of IGF-I on aggregation and on invasion could be mimicked by 1 microgram ml-1 insulin, but not by 0.5 microgram ml-1 IGF-II. The insulin effects were presumably not mediated by the IGF-I receptor, since they could not be blocked by an antibody against this receptor (alpha IR3). Our results indicate that IGF-I activates the invasion suppressor role of E-cadherin in MCF-7/6 cells.