Dielectric relaxation and conduction mechanism in Aurivillius ceramic Bi5Ti3FeO15

For this study, we synthesized Aurivillius Bi5Ti3FeO15 ceramic using the generic solid-state reaction route and then performed room-temperature X-ray diffraction to confirm that the compound had a single phase with no impurities. The surface morphology of the prepared sample was observed to contain microstructural grains approximately 0.2–2 μm in size. The dielectric properties of the sample were determ-ined as a function of frequency in a range of approximately 100 Hz to 1 MHz at various temperatures (303 K ≤ T ≤ 773 K). Nyquist plots of the impedance data were found to exhibit a semi-circular arc in the high-temperature region, which is explained by the equivalent electrical circuit (R1C1)(R2QC2), where R1 and R2 represent the resistances associated with the grains and grain boundaries, respectively, C1 and C2 are the re-spective capacitances, and Q is the constant phase element (CPE), which accounts for non-Debye type of behavior. Our results indicate that both the resistance and capacitance of the grain boundaries are more prominent than those of the grains. The alternating current (ac) conductiv-ity data were analyzed based on the Jonscher universal power law, which indicated that the conduction process is dominated by the hopping mechanism. The calculated activation energies of the relaxation and conduction processes were very similar (0.32 to 0.53 eV), from which we conclude that the same type of charge carriers are involved in both processes.     

Effect of Co substitution on the structural,dielectric and optical properties of KBiFe2O5

Cobalt (Co)-modified brownmillerite KBiFe2O5 (KBFO; [KBiFe2(1?x)Co2xO5 (x = 0, 0.05)]) polycrystalline is synthesized following the solid-state reaction route. Rietveld refinement of X-ray diffraction data confirmed the phase purity of KBFO and KBiFe1.9Co0.1O5 (KBFCO). The optical bandgap energy (Eg) of KBFO decreased from 1.59 to 1.51 eV because of Co substitution. The decrease in bandgap can be attributed to the tilting of the Fe–O tetrahedral structure of KBFCO. The observed room-temperature Raman peaks of KBFCO shifted by 3 cm?1 toward a lower wavenumber than that of KBFO. The shift in Raman active modes can be attributed to the change in the bond angles and bond lengths of the Fe–O tetrahedral structure and modification in response to oxygen deficiency in KBFO because of Co doping. Compared with that of KBFO, the frequency-dependent dielectric constant and dielectric loss of KBFCO decrease at room temperature, which is a con-sequence of the reduction in oxygen migration and modification in response to vibrational modes present in the sample.     

生产成本信息不对称下零售商风险厌恶的回购契约

探索在市场价格随机条件下,生产成本信息不对称零售商风险厌恶时,采用回购契约协调二级供应链的内在规律.构建新的条件下的回购契约模型并求解,分析信息不对称和风险厌恶对供应链上各决策变量的影响.通过算例仿真进行了验证,研究结果发现:在市场价格随机条件下,不管生产成本信息是否对称,只要零售商存在风险厌恶,供应链上各决策变量都会发生分岔突变的现象;不管零售商是否风险厌恶,生产成本信息不对称都会给供应商带来额外的收益,但会损害零售商与整个供应链的收益;信息越不对称,供应链上的各种决策变量在分岔突变区域的振幅越大.结论是:分岔突变现象是价格随机条件下,参与者风险厌恶时存在的一种特有现象;供应商能够通过隐瞒私人信息带来额外的收益,但损害零售商和供应链的利益;零售商应对生产成本信息不对称的最好办法就是以最低的成本使生产成本信息透明;零售商以平稳的心态面对各种外部风险,更有利于科学决策.     

Intrinsically disordered proteins in crowded milieu: when chaos prevails within the cellular gumbo

Effects of macromolecular crowding on structural and functional properties of ordered proteins, their folding, interactability, and aggregation are well documented. Much less is known about how macromolecular crowding might affect structural and functional behaviour of intrinsically disordered proteins (IDPs) or intrinsically disordered protein regions (IDPRs). To fill this gap, this review represents a systematic analysis of the available literature data on the behaviour of IDPs/IDPRs in crowded environment. Although it was hypothesized that, due to the excluded-volume effects present in crowded environments, IDPs/IDPRs would invariantly fold in the presence of high concentrations of crowding agents or in the crowded cellular environment, accumulated data indicate that, based on their response to the presence of crowders, IDPs/IDPRs can be grouped into three major categories, foldable, non-foldable, and unfoldable. This is because natural cellular environment is not simply characterized by the presence of high concentration of “inert” macromolecules, but represents an active milieu, components of which are engaged in direct physical interactions and soft interactions with target proteins. Some of these interactions with cellular components can cause (local) unfolding of query proteins. In other words, since crowding can cause both folding and unfolding of an IDP or its regions, the outputs of the placing of a query protein to the crowded environment would depend on the balance between these two processes. As a result, and because of the spatio-temporal heterogeneity in structural organization of IDPs, macromolecular crowding can differently affect structures of different IDPs. Recent studies indicate that some IDPs are able to undergo liquid–liquid-phase transitions leading to the formation of various proteinaceous membrane-less organelles (PMLOs). Although interiors of such PMLOs are self-crowded, being characterized by locally increased concentrations of phase-separating IDPs, these IDPs are minimally foldable or even non-foldable at all (at least within the physiologically safe time-frame of normal PMLO existence).     

Protein kinase D inhibitor CRT0066101 suppresses bladder cancer growth in vitro and xenografts via blockade of the cell cycle at G2/M

The protein kinase D (PKD) family of proteins are important regulators of tumor growth, development, and progression. CRT0066101, an inhibitor of PKD, has antitumor activity in multiple types of carcinomas. However, the effect and mechanism of CRT0066101 in bladder cancer are not understood. In the present study, we show that CRT0066101 suppressed the proliferation and migration of four bladder cancer cell lines in vitro. We also demonstrate that CRT0066101 blocked tumor growth in a mouse flank xenograft model of bladder cancer. To further assess the role of PKD in bladder carcinoma, we examined the three PKD isoforms and found that PKD2 was highly expressed in eight bladder cancer cell lines and in urothelial carcinoma tissues from the TCGA database, and that short hairpin RNA (shRNA)-mediated knockdown of PKD2 dramatically reduced bladder cancer growth and invasion in vitro and in vivo, suggesting that the effect of the compound in bladder cancer is mediated through inhibition of PKD2. This notion was corroborated by demonstrating that the levels of phospho-PKD2 were markedly decreased in CRT0066101-treated bladder tumor explants. Furthermore, our cell cycle analysis by flow cytometry revealed that CRT0066101 treatment or PKD2 silencing arrested bladder cancer cells at the G2/M phase, the arrest being accompanied by decreases in the levels of cyclin B1, CDK1 and phospho-CDK1 (Thr161) and increases in the levels of p27^Kip1 and phospho-CDK1 (Thr14/Tyr15). Moreover, CRT0066101 downregulated the expression of Cdc25C, which dephosphorylates/activates CDK1, but enhanced the activity of the checkpoint kinase Chk1, which inhibits CDK1 by phosphorylating/inactivating Cdc25C. Finally, CRT0066101 was found to elevate the levels of Myt1, Wee1, phospho-Cdc25C (Ser216), Gadd45α, and 14-3-3 proteins, all of which reduce the CDK1-cyclin B1 complex activity. These novel findings suggest that CRT0066101 suppresses bladder cancer growth by inhibiting PKD2 through induction of G2/M cell cycle arrest, leading to the blockade of cell cycle progression.     

具预警功能的可修复系统解的存在唯一性

针对可修复系统的预警功能,研究了其两不同部件并联可修复系统,运用泛函分析方法及C0-半群理论,给出非负时间依赖弱解的存在唯一性证明,为进一步研究系统解的逼近、主算子的谱性质等一系列问题提供参考。     

Histone acetylation dynamics regulating plant development and stress responses

Cellular and Molecular Life Sciences - Crop productivity is directly dependent on the growth and development of plants and their adaptation during different environmental stresses. Histone...     

A new twist to the No Miracles Argument for the success of science

J. D. Trout has recently developed a new defense of scientific realism, a new version of the No Miracles Argument. I critically evaluate Trout's novel defense of realism. I argue that Trout's argument for scientific realism and the related explanation for the success of science are self-defeating. In the process of arguing against the traditional realist strategies for explaining the success of science, he inadvertently undermines his own argument.