A High Order Bound Preserving Finite Difference Linear Scheme for Incompressible Flows

We propose a high order finite difference linear scheme combined with a high order bound preserving maximum-principle-preserving (MPP) flux limiter to solve the incompressible flow system. For such problem with highly oscillatory structure but not strong shocks, our approach seems to be less dissipative and much less costly than a WENO type scheme, and has high resolution due to a Hermite reconstruction. Spurious numerical oscillations can be controlled by the weak MPP flux limiter. Numerical tests are performed for the Vlasov-Poisson system, the 2D guiding-center model and the incompressible Euler system. The comparison between the linear and WENO type schemes, with and without the MPP flux limiter, will demonstrate the good performance of our proposed approach.     

Mimengosides J and K: two new neuroprotective triterpenoids from the fruits of Buddleja lindleyana

Two new 11-methoxyl substituted triterpenoids, named as mimengosides J (1) and K (2), along with seven known compounds, were isolated from the fruits of Buddleja lindleyana. Their structures were elucidated on the basis of spectroscopic analysis. In addition, the new ones were evaluated for protective effects against damage of SH-SY5Y cells induced by 1-methyl-4-phenylpyridinium ion (MPP⁺) and the results indicated that those may be one of the candidate compositions of Buddleja lindleyana for the treatment of neurodegenerative disease.

     

Cell cycle dependent intracellular distribution of two spliced isoforms of TCP/ILF3 proteins

TCP80 is an approximately 80kDa mammalian cytoplasmic protein that binds to a set of mRNAs and inhibits their translation in vitro and ex vivo. This protein has high sequence similarity to interleukin-2 enhancer-binding factors (NF90/ILF3) and the M-phase phosphoprotein (MPP4)/DRBP76. A 110kDa immunologic isoform of TCP80/NF90/MPP4/DRBP76, termed TCP110, also is present in cytoplasm and nuclei of many types of cells. A cDNA sequence coding for TCP110 was derived by 5(')RACE. The TCP110 sequence is identical to ILF3. The gene coding for TCP110/ILF3 mapped to human chromosome 19 and the gene organization was analyzed using TCP80 and TCP110/ILF3 cDNA sequences. The TCP/ILF3 gene spans >34.8kb and contains 21 exons. At least one alternatively spliced product involving exons 19-21 exists and predicts the formation of either TCP80 or TCP110/ILF3. However, the functional relationships of TCP80 and TCP110/ILF3 required elucidation. The metabolic turnover rates and subcellular distribution of TCP80 and TCP110/ILF3 during the cell cycle showed TCP80 to be relatively stable (t(1/2)=5 days) in the cytoplasmic compartment. In comparison, TCP110/ILF3 migrated between the cytoplasmic and nuclear compartments during the cell cycle. The TCP110 C-terminal segment contains an additional nuclear localizing signal that plays a role in its nuclear translocation. This study indicates that the multiple cellular functions, i.e., translation control, interleukin-2 enhancer binding, or cell division, of TCP/ILF3 are fulfilled by alternatively spliced isoforms.     

1—甲基—4—苯基吡啶啶离子诱发大鼠小脑颗粒细胞凋亡

目的 建立1－甲基－4－苯基吡啶离子（1－methy1-4-phenyl pyridinium ion,MPP^ )诱导的大鼠小脑颗粒细胞凋亡模型。方法 MPP^ 处理大鼠小脑颗粒细胞,分别用甲基绿－派诺宁染色,DNA凝胶电泳,流式细胞术进行检测。结果 浓度为50μmol/L MPP^ 使小脑颗粒细胞发生凋亡。结论 以MPP^ 为诱导剂建立的大鼠小脑颗粒细胞凋亡模型,可用于研究和帕金森病（PD）有关的细胞凋亡的调控机制和筛选抗PD药物。     

EGb对MPP^＋诱导的PC12细胞凋亡的影响

目的 观察EGb对MPP^ 诱导的PC12细胞凋亡的细胞。方法 MPP^ 诱导PC12细胞凋亡,AO／EB染色,荧光显微镜下观察凋亡细胞。结果 EGb50、100μg/ml在6h、12h、24h可抑制细胞凋亡,而EGb25μg/ml则无效。结论 EGb在6h、12h、24h时呈剂量依赖性降低细胞凋亡率,提示EGb有可能通过抑制DA能神经元凋亡而相对增加DA含量。     

抗氧化作用可能是人参皂甙Rg1抗细胞凋亡的机制

目的 :探讨人参皂甙Rg1对MPP+诱导SHSY5Y细胞凋亡的保护作用及其可能的机制。方法 :用吖啶橙溴化乙锭染色观察SHSY5Y细胞凋亡率 ,流式细胞仪检测线粒体跨膜电位及细胞内活性氧 (ROS)水平 ,WesternBlot法检测bcl 2、bax蛋白表达水平。结果 :经 10 μmol·L- 1Rg1预处理后 ,MPP+诱导的SHSY5Y细胞凋亡受到明显的抑制 ,虽然线粒体跨膜电位无明显改变 ,但细胞内ROS下降 ,而bcl 2蛋白表达水平增加 ,bax蛋白表达水平减少。结论 :Rg1可抑制MPP+诱导的SHSY5Y细胞凋亡 ,其作用机制可能是通过清除ROS、调节bcl 2、bax蛋白表达水平起作用。     

伊拉地平对 MPP＋损伤 PC12细胞保护作用的实验研究

目的：研究伊拉地平（ ISR ）对1-甲基-4-苯基吡啶离子（ MPP＋）损伤的PC12细胞的保护作用及可能机制。方法MPP ＋处理PC12细胞建立帕金森病细胞模型;4-甲基偶氮唑蓝（ MTT）比色法检测细胞存活率;双氯荧光黄乙酸乙酯（ DCFH-DA）染色流式细胞术检测细胞内活性氧（ ROS）的生成;JC-1染色流式细胞术检测细胞线粒体膜电位（ MMP）。结果1 mmol · L－1MPP＋处理PC12细胞24 h后能明显抑制细胞生长（P＜0．01）;降低线粒体膜电位;ROS含量增加。2μmol· L－1伊拉地平预处理后, PC12细胞存活率显著增加（ P＜0．01）;线粒体膜电位升高;ROS生成减少。结论伊拉地平对MPP＋损伤的PC12细胞具有保护作用,其作用机制可能与维持线粒体正常膜电位,稳定线粒体功能,阻止线粒体氧化应激发生有关。