三端口四态变量CNN原理在肿瘤生长方程中应用

提出了一种在抗癌免疫监视下的肿瘤生长细胞神经网络(GIsAC CNN)模型.用具有3个端口4个态变量CNN的解析判别法研究了GusAC CNN的分歧图.数值模拟了癌细胞扩散和清除过程.研究结果似乎表明:效应细胞对癌细胞的清除起着至关重要作用,细胞组织中存在免疫缺陷,可能导致癌细胞的转移与扩散.     

细胞凋亡与肿瘤治疗

细胞凋亡与许多疾病特别是肿瘤的发生发展有关，许多癌基因与抑癌基因参与细胞凋亡过程。对细胞凋亡以及在肿瘤治疗中的有关系进行了综述。     

5种细胞周期调控基因在小鼠生殖细胞发育过程中的表达研究

 以成熟(10周龄以上)的昆明种正常小鼠的精巢和卵巢为材料,利用地高辛标记的基因探针进行组织切片上的DNA-mRNA分子原位杂交,研究了PCNA,cdc2,cyclin D1,p2 1和 p16 5种细胞周期调控基因在生殖细胞发育过程中的表达.结果表明:PCNA基因在睾丸组织的精原细胞和精母细胞中有强杂交信号,而在雌性生殖细胞及滤泡细胞的发育过程都没有杂交信号;cyclin D1,cdc2,p2 1,p16基因在生殖细胞的发育过程中都没有,表明这些基因并没有参与小鼠生殖细胞的生长和分化调控.这些事实表明在生殖细胞发育过程中,控制细胞增殖和增殖抑制的基因与培养细胞有不同的机制,它们可能采用了不同的调控系统.     

多晶硅太阳电池的有效等离子体氢钝化

文章报道了一种用于多晶硅太阳电池氢纯化的简单试验装置，等离子体氢是通过辉光放电方法产生。三类完成电极制作的多晶硅太阳电池用于氢纯化试验，伏安特性测试结果表明，经过等离子体氢纯化后的太阳电池性能都有所提高，电池的光电转换效率相对改善高达10.6%。     

卵巢环状小管性索瘤的临床病理分析

对38例（本院2周及国内文献36例）卵巢太小管性索瘤从临床、病理和激素分泌等方面进行分析，年龄4－60岁，平均23岁。主要临床表现为：内分泌功能紊乱（性早熟，月经不规则及绝经后出血）和腹部肿块，仅1例伴有口唇粘膜黑色素沉着－－胃肠道息肉综合征；特征性组织学结构为：单层或复层环状小管，管周有基底膜样结构。此病属于低度恶性肿瘤，并对此病的组织来源进行了讨论。     

大鼠肝细胞核仁超微结构与rDNA分布位点

以常规电镜及NAMA－Ur DNA特异染色技术对Wistar大鼠肝细胞核仁的超微结构和rRNA的分布进行了观察。常规电镜技术表明大鼠肝细胞核仁纤维中心（FC）是电子透明区，数量较多，形状不规则。密集纤维组分（DFC）是围绕FC的环状结构部分，电子密度很高。FC中的染色质存在着一个介于集缩和解集缩状态之间的变化过程。NAMA－Ur DNA特异染色技术表明核仁内rDNA呈分散性分布，主要分布于DFC中（包括FC）的边缘），同时观察到与核仁相随染色质相连的核仁内rDNA呈念珠状结构。     

二氧化硫对小鼠骨髓细胞微核的诱发及沙棘油的防护作用

研究了大气中二氧化硫 (SO2 )污染物的遗传毒理效应。采用 SO2 吸入染毒法 ,模拟 SO2 大气污染 ,从整体水平直接对短期与长期 SO2 吸入诱发小鼠骨髓嗜多染红细胞 (PCE)形成微核 (MN)的效应及沙棘油的防护作用进行了研究。结果表明 :(1)短期与长期 SO2 吸入均可引起小鼠骨髓 PCE细胞微核率和微核细胞率显著升高 ,且有明确的剂量 -效应关系 ;(2 )随着吸入的 SO2 浓度的增高 ,不仅单微核细胞率 ,而且双微核细胞率均显著升高 ;(3) SO2对阳性致突变剂乌拉坦诱发微核的作用有显著抑制效应 ;(4 )沙棘油对 SO2 诱发 PCE微核的效应有防护作用。从此可以结论 :SO2 空气污染物是哺乳类细胞染色体断裂剂和基因毒性因子、SO2 与阳性致突变剂的联合作用是复杂的 ,某些天然物质对 SO2 的毒效应有防护作用     

胚胎干细胞的培养体系综述

综述胚胎干细胞培养基，有饲养层培养体系和无饲养层培养体系的主要成分，以及无血清胚胎干细胞培养基。     

Hydrogen Production with High Evolution Rate and High Yield by Immobilized Cells of Hydrogen-producing Bacteria Strain B49 in a Column Reactor

To improve the hydrogen evolution rate in continuous hydrogen production of a novel fermentative hydrogen-producing bacteria strain B49 (AF481148 in EMBL), 4 % immobilized cells by polyvinyl alcohol-boric acid method, with the addition of a small amount of calcium alginate in a column reactor obtain hydrogen yield of 2.31 mol H2/mol glucose and hydrogen evolution rate of 1435.4 ml/L culture*h respectively at medium retention time of 2.0 h with a medium containing 10g glucose/L. Moreover, as the cell density in gel beads is increased to 8%, hydrogen yield and hydrogen evolution rate for 10g glucose/L are 2.34 mol H2/mol glucose and 2912.4 ml/L culture*h respectively at medium retention time of 1.0 h, and for molasses wastewater COD of 7505.9 mg/L hydrogen production potential of 205.6 ml/g COD and hydrogen evolution rate of 2057.7 ml/L culture*h at hydraulic retention time of 0.75 h are observed. In the continuous culture pH value keeps around 3.9 by self-regulating.     

Genistein inhibits human TNF-α-induced porcine endothelial cell adhesiveness for human monocytes and natural killer cells

Cellular immune response is a major barrier to xenotransplantation. Human tumor necrosis factor-α (hTNF-α) possesses cross-species activity and directly amplifies the immune rejection via the upregulation of adhesion molecules on porcine endothelium. We investigated the role of protein tyrosine phosphorylation in the induction of expression of E-sclectin and vascular cell adhesion molecule-1 (VCAM-1), and the augmentation of adhesion of human peripheral blood monocytes (PBMo) and natural killer cells (PBNK), after rhTNF-α-stimulation of porcine aortic endothelial cells (PAEC) in vitro, rhTNF-α-increased adhesiveness of PAEC for both PBMo and PBNK was dose-dependently reduced by pretreatment of PAEC with the selective protein tyrosine kinase (PTK) inhibitor genistein. The inhibitory effect occurred at the early time of PAEC activation triggered by rhTNF-α, and was completely reversible. PTK activity assay indicated that genistein also suppressed rhTNF-α stimulated activation of protein tyrosine kinases (PTKs) in PAEC in a dose-dependent manner. Flow cytometric analysis showed that genistein inhibited the upregulation of E-selectin and VCAM-1 by rhTNF-α. These results suggest that PTKs may regulate the expression of E-selectin and VCAM-1 on PAEC and the adherence of PBMo and PBNK induced by rhTNF-α. Moreover, dietary genistein, used as an adhesion antagonist, may contribute to managing the cell-mediated rejection in the clinical application.