Mechanism Of Cooperative Interaction Research Articles

Real-Time Energy-Saving Optimization for Multiple Trains Based on Multiagent Cooperative Control

Nowadays, the energy-saving optimization problem has gradually become a hot spot in the subject of high-speed train control. Traditional static train trajectory planning is designed offline according to a preplanned timetable, but ignored are the uncertainties of parameters because of line conditions and other factors in the process of operation. Thus, the previous operation strategy may not suit the remaining section. The cooperative control strategy for multiple trains was investigated with the aim of conserving energy between successive stations under the constraints of safety and punctuality. First, combined with the train operation strategy under the quasi-moving block system of the Chinese Train Control System, a train cooperative interaction mechanism based on multiagent input is proposed to obtain the real-time running characteristics of trains on the railway via the Radio Block Center (RBC) agent. In the case of unanticipated events of railway line conditions, train operation is often out of accord with the timetable. Therefore, a resilience set related to trip-time deviation and headway variation is introduced to evaluate the robustness of the railway system and achieve balance in the train group. Also, a multigroup parallel differential evolution algorithm is developed to solve the online optimization problem of a high-speed train group according to real-time information. The proposed approach is analyzed by using operational data from the Wuhan–Changsha highspeed railway line in China to assess energy savings and punctuality. Results of the case study show superior performance and effectiveness of the model, and the methodology is illustrated.

The interaction of p53 with 3'-terminal mismatched DNA

The diversity of p53 functions involves its interaction with sequence-specific, non-sequence-specific and various damaged sites in DNA. The preferential excision of misincorporated over correct nucleotides by the 3′→5′ exonuclease activity of p53 provides a molecular basis for p53 involvement in the correction of the DNA replication errors. However, p53 exhibits variations in its comparative efficiency to excise different 3'-terminal mismatched nucleotides. To determine the importance of the binding capacity of the protein to various 3'-terminal damaged sites, we have examined the interaction of p53 with linear dsDNAs containing various 3'-terminal mismatches, employing a gel retardation assay. The data demonstrate the intrinsic 3'-terminal mismatched DNA binding capacity of p53. Since p53 binds directly to various 3'-terminal purine:pyrimidine and purine:purine mispairs to an equal extent, p53 can be considered as a general 3'-mismatched DNA binding protein. Apparently, 3'-terminal mismatched bases are structural element to which p53 can bind, that extends the spectrum of damage sites to which p53 may respond. The formation of the p53-mismatched DNA complex is independent of the sequence context. Thus, the dissimilarities in mispair excision efficiency are probably due to an inherent property of the p53 in excision of 3'-mismatched nucleotides by a bound protein. The results establish a framework for understanding the mechanism of cooperative interaction between p53 and exonuclease-deficient DNA polymerase (e.g. HIV-1 RT). Within the context of error-correction events, p53 by recognition and excision of 3'-mismatched nucleotides from DNA, may be involved in DNA repair, thus increasing the accuracy of DNA synthesis by DNA polymerases.

Cooperative Processes in Nd3☎/Yb3☎ Co-Doped Yag Nanocrystallites

The cooperative processes in doubly doped Nd/Yb:YAG nanocrystallites were investigated. An extremely strong Yb3☎ ion concentration influence on absorption intensities was noticed. An efficient Nd3☎ → Yb3☎ energy transfer in YAG nanocrystallites was found. However no back transfer was observed. The mechanisms of cooperative interactions between Nd3☎ and Yb3☎ ions in YAG nanocrystallites responsible for the observed concentration effects are discussed.

Molecular Symmetry Breaking and Chiral Expression of Discotic Liquid Crystals in Two-Dimensional Systems

We have studied the self-assembled monolayers from a series of discotic liquid crystal molecules on graphite substrate using scanning tunneling microscopy. An emergence of chirality in 1,7,13-trialkanoyldecacyclene (with n-carbon side chains, n = 14) monolayers was observed in the assembly. The driving force of the assembling behavior could be related to a cooperative interaction mechanism, possibly due to intermolecular steric hindrance, two-dimensional crystallization of alkyl substitutents.

σ Bond Activation by Cooperative Interaction with ns2 Atoms: Be + nH2, n = 1−3

Ab initio investigations at the MP2, CCSD(T), and MRCISD levels of theory with augmented triple-ζ basis sets have identified and characterized various stationary points on the Be/(H2)n, n = 1−3, hypersurfaces. The van der Waals complexes, Be(H2)n, are very weakly bound (De = 0.08−0.32 kcal/mol with respect to H2 loss) with H2/H2 interactions playing an important role in determining equilibrium structures which can be understood in terms of the various relevant long-range potentials. The covalent molecule, BeH2, is found to have a linear, centrosymmetric structure and to be strongly bound with respect to Be + H2, in agreement with previous calculations. BeH2 interacts weakly with additional H2 molecules (De < 0.75 kcal/mol) which are positioned parallel to the near-linear BeH2 moiety in the equilibrium structures of the BeH2(H2)n-1 complexes. Of particular interest is the dramatic change in the nature of the transition state for BeH2 production depending on the number of H2 molecules present. For n = 1, the reaction proceeds stepwise: first breaking the H2 bond and forming one BeH bond followed by forming the second BeH bond. This process has an activation energy of about 56 kcal/mol. For n = 2, the reaction proceeds via a pericyclic mechanism through a planar cyclic transition state where two H2 bonds are broken while simultaneously two BeH bonds and one new H2 bond are formed. The activation energy for this process decreases from the n = 1 value to about 38 kcal/mol. For n = 3, the reaction proceeds through a true insertion mechanism with the addition of the third H2 molecule, decreasing the activation energy to about 33 kcal/mol. The results are discussed in comparison to the isoelectronic B+/nH2 systems where significant σ bond activation through a cooperative interaction mechanism has been identified.

Ab initio investigations of Li−+nH2→LiH2−(H2)n−1,n=1–3

Ab initio investigations at the coupled-cluster single double (triple) [CCSD(T)] and MRCISD level with augmented triple and quadruple zeta basis sets have identified various stationary points on the Li−/(H2)n,n=1–3, hypersurfaces. The electrostatic complexes, Li−(H2)n, are very weakly bound (De&amp;lt;0.25 kcal/mol with respect to H2 loss) and H2/H2 interactions play a contributing role in determining the equilibrium structures within the electrostatic constraint of a linear or near-linear Li−–H–H orientation. The covalent molecular ion, LiH2−, is found to have a linear centrosymmetric structure and to be bound with respect to Li−+H2 in agreement with previous calculations. The interaction of LiH2− with additional H2 is purely electrostatic but with a De larger than those of the Li−(H2)n complexes. LiH2−(H2) is found to have a linear equilibrium structure and LiH2−(H2)2 is found to have two almost isoenergetic structures: linear with an H2 on either end of the LiH2−, and C2v with both H2 on the same end of the LiH2−. Of particular interest is the dramatic change in the nature of the transition state for LiH2− production depending on the number of H2 molecules present. For n=1, the reaction proceeds through a conical intersection between the lowest energy B21 and A11 electronic surfaces in C2v symmetry. For n=2, the reaction occurs on a single surface in a pericyclic mechanism through a transition state consisting of a planar five-member ring where simultaneously two H2 bonds are broken while two LiH bonds and one new H2 bond are formed. For n=3, the reaction proceeds by direct insertion of Li− into one of the H2 molecules with the two additional H2 molecules providing substantial stabilization of the transition state by taking on part of the negative charge in a weakly covalent interaction. The results are discussed in comparison to the isoelectronic B+/(H2)n systems where significant sigma bond activation through a cooperative interaction mechanism has been identified recently.

Transport and Pharmacological Properties of Nine Different Human Na,K-ATPase Isozymes

Na,K-ATPase plays a crucial role in cellular ion homeostasis and is the pharmacological receptor for digitalis in man. Nine different human Na,K-ATPase isozymes, composed of 3 alpha and beta isoforms, were expressed in Xenopus oocytes and were analyzed for their transport and pharmacological properties. According to ouabain binding and K(+)-activated pump current measurements, all human isozymes are functional but differ in their turnover rates depending on the alpha isoform. On the other hand, variations in external K(+) activation are determined by a cooperative interaction mechanism between alpha and beta isoforms with alpha2-beta2 complexes having the lowest apparent K(+) affinity. alpha Isoforms influence the apparent internal Na(+) affinity in the order alpha1 > alpha2 > alpha3 and the voltage dependence in the order alpha2 > alpha1 > alpha3. All human Na,K-ATPase isozymes have a similar, high affinity for ouabain. However, alpha2-beta isozymes exhibit more rapid ouabain association as well as dissociation rate constants than alpha1-beta and alpha3-beta isozymes. Finally, isoform-specific differences exist in the K(+)/ouabain antagonism which may protect alpha1 but not alpha2 or alpha3 from digitalis inhibition at physiological K(+) levels. In conclusion, our study reveals several new functional characteristics of human Na,K-ATPase isozymes which help to better understand their role in ion homeostasis in different tissues and in digitalis action and toxicity.

Tumor necrosis factor induces enhanced responses to platelet‐activating factor and differentiation in human monocytic Mono Mac 6 cells

Human Mono Mac 6 cells exhibit characteristics of mature blood monocytes. Treatment of these cells with human recombinant human tumor necrosis factor (TNF) resulted in an increase in phagocytosis and phorbol myristate acetate-stimulated superoxide anion production at 12 h and growth retardation occurring at 24 h. Moreover, TNF induced a moderate increase of CD14 surface antigen expression, used as a phenotypic marker of monocyte/macrophage differentiation. Platelet-activating factor (PAF) stimulated a rapid rise in cytosolic free Ca++ ([Ca++]i) of 308 +/- 93 nM in TNF-treated cells compared to untreated cells (33 +/- 8 nM, n = 4). The effect of TNF was dose and time dependent, evident after 12 h and maximal at 48 h. The enhanced PAF-induced [Ca++]i rise was inhibited by the PAF receptor antagonist L-659,989 and EGTA, indicating receptor-dependent Ca++ influx. Furthermore, L-659,989 and PAF inhibited specific 3H-labeled PAF binding in TNF-treated, but not in untreated cells. Consistently, PAF stimulated arachidonic acid release only in TNF-treated cells. Preincubation of cells with anti-TNF monoclonal antibodies abolished TNF-induced effects, but failed to block lipopolysaccharide (LPS) effects. Distinct mechanisms of action by LPS were reflected by the different ability to induce surface antigen expression. In conclusion, the enhancement of PAF responses by TNF, associated with functional characteristics of differentiation in Mono Mac 6 cells, may represent a specific mechanism of cooperative interaction between PAF and TNF in inflammation, sepsis, immunoregulation and atherogenesis.