粉煤灰微波改性及其对甲基橙的吸附性能

将取自于热电厂的粉煤灰(FA)球磨5h得到超细粉煤灰(UFA),再经过微波处理得到微波辐照改性超细粉煤灰(MFA),并研究其对水溶液中甲基橙的吸附性能。动力学研究结果表明,改性粉煤灰对甲基橙的吸附符合二级吸附动力学模型,通过模型计算出的FA,UFA和MFA的二级吸附速率常数(k2)分别为9.30×10-3,13.00×10-3,18.35×10-3g.mg-1.min-1;热力学研究结果表明,吸附过程可以用Langmuir方程描述。计算吸附热力学参数ΔG,ΔS和ΔH,FA,UFA和MFA对甲基橙的吸附焓(ΔH)分别为-23.03,-25.98和-29.42kJ·mol-1。ΔG和ΔH均为负值,表明吸附为一自发的放热过程。     

利用张力样条模拟定向井井眼轨迹的方法研究

根据张力样条的特性及定向井井眼轨迹的形成规律,提出了用张力样条模拟定向井井眼轨迹的方法.详细介绍了用张力样条法确定定向井井眼轨迹的步骤.利用这种方法可以计算定向井任一点的空间位置.实例计算结果表明,在已知任意个相邻测点之间,用张力样条插值计算未知测点的井斜角和方位角,与实测值相比,误差很小,满足实际井眼轨迹计算的要求,具有实用价值,为定向井井眼轨迹的计算提供了一种新的方法.     

Antiviral activity of some derivatives of 2-styrylquinoline

Zusammenfassung In Mäuseversuchen wurde gezeigt, dass gewisse Styrylquinoline in vivo eine Wirkung gegen Semliki-Forest-Virus haben.     

Suppression of polyglutamine-mediated neurodegeneration in Drosophila by the molecular chaperone HSP70

At least eight inherited human neurodegenerative diseases are caused by expansion of a polyglutamine domain within the respective proteins. This confers dominant toxicity on the proteins, leading to dysfunction and loss of neurons. Expanded polyglutamine proteins form aggregates, including nuclear inclusions (NI), within neurons, possibly due to misfolding of the proteins. NI are ubiquitinated and sequester molecular chaperone proteins and proteasome components, suggesting that disease pathogenesis includes activation of cellular stress pathways to help refold, disaggregate or degrade the mutant disease proteins. Overexpression of specific chaperone proteins reduces polyglutamine aggregation in transfected cells, but whether this alters toxicity is unknown. Using a Drosophila melanogaster model of polyglutamine disease, we show that directed expression of the molecular chaperone HSP70 suppresses polyglutamine-induced neurodegeneration in vivo. Suppression by HSP70 occurred without a visible effect on NI formation, indicating that polyglutamine toxicity can be dissociated from formation of large aggregates. Our studies indicate that HSP70 or related molecular chaperones may provide a means of treating these and other neurodegenerative diseases associated with abnormal protein conformation and toxicity.     

Identification of Stk6/STK15 as a candidate low-penetrance tumor-susceptibility gene in mouse and human

Linkage analysis and haplotype mapping in interspecific mouse crosses (Mus musculus x Mus spretus) identified the gene encoding Aurora2 (Stk6 in mouse and STK15 in human) as a candidate skin tumor susceptibility gene. The Stk6 allele inherited from the susceptible M. musculus parent was overexpressed in normal cells and preferentially amplified in tumor cells from F(1) hybrid mice. We identified a common genetic variant in STK15 (resulting in the amino acid substitution F31I) that is preferentially amplified and associated with the degree of aneuploidy in human colon tumors. The Ile31 variant transforms rat1 cells more potently than the more common Phe31 variant. The E2 ubiquitin-conjugating enzyme UBE2N was a preferential binding partner of the 'weak' STK15 Phe31 variant form in yeast two-hybrid screens and in human cells. This interaction results in colocalization of UBE2N with STK15 at the centrosomes during mitosis. These results are consistent with an important role for the Ile31 variant of STK15 in human cancer susceptibility.     

On robust estimation of threshold autoregressions

We investigate the effects of additive outliers on the least squares (LS) estimation of threshold autoregressive models. The class of generalized-M (GM) estimates for linear time series is modified and applied to non-linear threshold processes. A Monte Carlo experiment is carried out to study the robust properties of these estimates. Their relative forecasting performances are also examined. The results indicate that the GM method is preferable to the LS estimation when the observations are contaminated by additive outliers. A real example is also given to illustrate the proposed method.     

Cyclic CMP (cytidine 3',5'-monophosphate) suppresses changes in human sperm amplitude of lateral head displacement and hyperactivation

The dibutyryl analog of cCMP suppressed sperm amplitude of lateral head displacement and hyperactivation. Sperm motility was inhibited by dibutyryl cCMP with a shift toward less linear trajectory sperm movements. The results suggest a role of cCMP as an inhibitory signal on sperm motility patterns related to sperm capacitation.     

cAMP initiates early phase neuron-like morphology changes and late phase neural differentiation in mesenchymal stem cells

The intracellular second messenger cAMP is frequently used in induction media to induce mesenchymal stem cells (MSCs) into neural lineage cells. To date, an understanding of the role cAMP exerts on MSCs and whether cAMP can induce MSCs into functional neurons is still lacking. We found cAMP initiated neuron-like morphology changes early and neural differentiation much later. The early phase changes in morphology were due to cell shrinkage, which subsequently rendered some cells apoptotic. While the morphology changes occurred prior to the expression of neural markers, it is not required for neural marker expression and the two processes are differentially regulated downstream of cAMP-activated protein kinase A. cAMP enabled MSCs to gain neural marker expressions with neuronal function, such as, calcium rise in response to neuronal activators, dopamine, glutamate, and potassium chloride. However, only some of the cells induced by cAMP responded to the three neuronal activators and further lack the neuronal morphology, suggesting that although cAMP is able to direct MSCs towards neural differentiation, they do not achieve terminal differentiation.     

14-3-3Sigma is required to prevent mitotic catastrophe after DNA damage.

14-3-3Sigma is a member of a family of proteins that regulate cellular activity by binding and sequestering phosphorylated proteins. It has been suggested that 14-3-3sigma promotes pre-mitotic cell-cycle arrest following DNA damage, and that its expression can be controlled by the p53 tumour suppressor gene. Here we describe an improved approach to the generation of human somatic-cell knockouts, which we have used to generate human colorectal cancer cells in which both 14-3-3sigma alleles are inactivated. After DNA damage, these cells initially arrested in the G2 phase of the cell cycle, but, unlike cells containing 14-3-3sigma, the 14-3-3sigma-/- cells were unable to maintain cell-cycle arrest. The 14-3-3sigma-/- cells died ('mitotic catastrophe') as they entered mitosis. This process was associated with a failure of the 14-3-3sigma-deficient cells to sequester the proteins (cyclin B1 and cdc2) that initiate mitosis and prevent them from entering the nucleus. These results may indicate a mechanism for maintaining the G2 checkpoint and preventing mitotic death.