The Logarithm Model of Development Power: A Tool to Analyze the Motivity of Economic Growth

After the discussions to exponential and power model [F. Dai, 2005], this paper points out there are three kinds of basic modes in the macroeconomic process, i.e., the exponential, power and logarithm mode, and discusses the logarithm model of Development Power (DP). By the analysis on logarithm model of DP, we will see the reasons, of which there are anomaly cycles in economic process, are just the alternate motion of DP accumulating and releasing. And that is also the reasons that there are the economic fluctuations in production markets. The logarithm model of DP can also describe the different characters of DP motion at the different stage, and indicates in analytic way that the diffusion of DP and the diversifications of economic productivity also might occur after an economic recession. The empirical researches are done about the conclusions in this paper, and the results express that the logarithm model is better than the power model and exponential model of DP in many cases. These three models of DP can not be replaced one another.Development Power (DP); Partial Distribution; logarithm model; macroeconomic analysis

Modification of Si(001) substrate bonding by adsorbed Ge or Si dimer islands

Journal ArticleHigh-resolution scanning tunneling microscopy studies of the Si(100)-(2 X 1) surface show a heretofore unrecognized distortion of the substrate structure when islands form during the initial stage of growth of either Si or Ge. The distortion, reflecting the influence of strain, extends at least three dimers away from the adsorption sites. We present a realistic structural model

Curcumin inhibits migration and invasion of non-small cell lung cancer cells through up-regulation of miR-206 and suppression of PI3K/AKT/mTOR signaling pathway

Curcumin has been proved to inhibit cell proliferation and induce cell apoptosis in non-small cell lung cancer (NSCLC). However, little is known about antimetastatic effects and molecular mechanisms of curcumin in NSCLC. In this study, we investigated the involvement of miR-206 in curcumin’s anti-invasion and anti-migration in NSCLC. Cell proliferation was determined by MTT assay. Cell migration and invasion were analyzed by wound healing assay and transwell assay. MiRNA-206 expression was detected by real-time PCR. Western blot was used to detect the protein expression of PI3K/AKT/mTOR signaling pathway. Curcumin significantly inhibited migration and invasion in A549 cells, accompanied by significantly elevated miR-206 expression. Overexpression of miR-206 could inhibit migration and invasion of A549 cells, but it could also significantly decrease the phosphorylation levels of mTOR and AKT. The inhibition of miR-206 promoted cell migration, invasion and increased the phosphorylation level of mTOR and AKT. Furthermore, miR-206 mimics improved the inhibitory effects of curcumin on cell migration, invasion and the phosphorylation level of mTOR and AKT in A549 cells. On the contrary, MiR-206 inhibitors reversed the inhibitory effects of curcumin on cell migration, invasion and the phosphorylation level of mTOR and AKT. In conclusion, curcumin inhibited cell invasion and migration in NSCLC by elevating the expression of miR-206 which further suppressed the activation of the PI3K/AKT/mTOR pathway

Low pH Potentiates Both Capsaicin Binding and Channel Gating of VR1 Receptors

Capsaicin ion channels are highly expressed in peripheral nervous terminals and involved in pain and thermal sensations. One characteristic of the cloned VR1 receptor is its multimodal responses to various types of noxious stimuli. The channel is independently activated by capsaicin and related vanilloids at submicromolar range, by heat above 40°C, and by protons at pH below 6.5. Furthermore, simultaneous applications of two or more stimuli lead to cross sensitization of the receptor, with an apparent increase in the sensitivity to any individual stimulus when applied alone. We studied here the mechanism underlying such cross-sensitization; in particular, between capsaicin and pH, two prototypical stimuli for the channel. By analyzing single-channel currents recorded from excised-patches expressing single recombinant VR1 receptors, we examined the effect of pH on burst properties of capsaicin activation at low concentrations and the effect on gating kinetics at high concentrations. Our results indicate that pH has dual effects on both capsaicin binding and channel gating. Lowering pH enhances the apparent binding affinity of capsaicin, promotes the occurrences of long openings and short closures, and stabilizes at least one of the open conformations of the channel. Our data also demonstrate that capsaicin binding and protonation of the receptor interact allosterically, where the effect of one can be offset by the effect of the other. These results provide important basis to further understand the nature of the activation pathways of the channel evoked by different stimuli as well as the general mechanism underling the cross-sensitization of pain