Better synchronizability predicted by a new coupling method

In this paper, inspired by the idea that the hub nodes of a highly heterogeneous network are not only the bottlenecks, but also effective controllers in the network synchronizing process, we bring forward an asymmetrical coupling method where the coupling strength of each node depends on its neighbors' degrees. Compared with the uniform coupled method and the recently proposed Motter-Zhou-Kurth method, the synchronizability of scale-free networks can be remarkably enhanced by using the present coupled method.Comment: 6 pages, 6 figures; to be published in EPJ

The two-pseudoscalar-meson decay of χcJ\chi_{cJ} with twist-3 corrections

The decays of $\chi_{cJ} \to \pi^+\pi^-, K^+K^-$ $(J=0,2)$ are discussed within the standard and modified hard scattering approach when including the contributions from twist-3 distribution amplitudes and wave functions of the light pseudoscalar meson. A model for twist-2 and twist-3 distribution amplitudes and wave functions of the pion and kaon with BHL prescription are proposed as the solution to the end-point singularities. The results show that the contributions from twist-3 parts are actually not power suppressed comparing with the leading-twist contribution. After including the effects from the transverse momentum of light meson valence-quark state and Sudakov factors, the decay widths of the $\chi_{cJ}$ into pions or kaons are comparable with the their experimental data.Comment: 31 pages, 5 figures, 3 table

Mobility enhancement and highly efficient gating of monolayer MoS2 transistors with Polymer Electrolyte

We report electrical characterization of monolayer molybdenum disulfide (MoS2) devices using a thin layer of polymer electrolyte consisting of poly(ethylene oxide) (PEO) and lithium perchlorate (LiClO4) as both a contact-barrier reducer and channel mobility booster. We find that bare MoS2 devices (without polymer electrolyte) fabricated on Si/SiO2 have low channel mobility and large contact resistance, both of which severely limit the field-effect mobility of the devices. A thin layer of PEO/ LiClO4 deposited on top of the devices not only substantially reduces the contact resistance but also boost the channel mobility, leading up to three-orders-of-magnitude enhancement of the field-effect mobility of the device. When the polymer electrolyte is used as a gate medium, the MoS2 field-effect transistors exhibit excellent device characteristics such as a near ideal subthreshold swing and an on/off ratio of 106 as a result of the strong gate-channel coupling.Comment: 17 pages, 4 figures, accepted by J. Phys.

Deletion or insertion in the first immunoglobulin-plexin-transcription (IPT) domain differentially regulates expression and tumorigenic activities of RON receptor Tyrosine Kinase

<p>Abstract</p> <p>Background</p> <p>Activation of the RON receptor tyrosine kinase, a member of the c-MET family, regulates tumorigenic phenotypes. The RON extracellular domains are critical in regulating these activities. The objective of this study was to determine the role of the first IPT domain in regulating RON-mediated tumorigenic activities and the underlying mechanisms.</p> <p>Results</p> <p>Two RON variants, RON160 and RON^E5/6inwith deletion and insertion in the first IPT domain, respectively, were molecularly cloned. RON160 was a splicing variant generated by deletion of 109 amino acids encoded by exons 5 and 6. In contrast, RON^E5/6inwas derived from a transcript with an insertion of 20 amino acids between exons 5 and 6. Both RON160 and RON^E5/6inwere proteolytically matured into two-chain receptor and expressed on the cell surface. RON160 was constitutively active with tyrosine phosphorylation. However, activation of RON^E5/6inrequired ligand stimulation. Deletion resulted in the resistance of RON160 to proteolytic digestion by cell associated trypsin-like enzymes. RON160 also resisted anti-RON antibody-induced receptor internalization. These features contributed to sustained intracellular signaling cascades. On the other hand, RON^E5/6inwas highly susceptible to protease digestion, which led to formation of a truncated variant known as RONp110. RON^E5/6inalso underwent rapid internalization upon anti-RON antibody treatment, which led to signaling attenuation. Although ligand-induced activation of RON^E5/6inpartially caused epithelial to mesenchymal transition (EMT), it was RON160 that showed cell-transforming activities in cell focus formation and anchorage-independent growth. RON160-mediated EMT is also associated with increased motile/invasive activity.</p> <p>Conclusions</p> <p>Alterations in the first IPT domain in extracellular region differentially regulate RON mediated tumorigenic activities. Deletion of the first IPT results in formation of oncogenic variant RON160. Enhanced degradation and internalization with attenuated signaling cascades could be the mechanisms underlying non-tumorigenic features of RON^E5/6in.</p

Ribosomal Protein S6 Kinase (RSK)-2 as a central effector molecule in RON receptor tyrosine kinase mediated epithelial to mesenchymal transition induced by macrophage-stimulating protein

<p>Abstract</p> <p>Background</p> <p>Epithelial to mesenchymal transition (EMT) occurs during cancer cell invasion and malignant metastasis. Features of EMT include spindle-like cell morphology, loss of epithelial cellular markers and gain of mesenchymal phenotype. Activation of the RON receptor tyrosine kinase by macrophage-stimulating protein (MSP) has been implicated in cellular EMT program; however, the major signaling determinant(s) responsible for MSP-induced EMT is unknown.</p> <p>Results</p> <p>The study presented here demonstrates that RSK2, a downstream signaling protein of the Ras-Erk1/2 pathway, is the principal molecule that links MSP-activated RON signaling to complete EMT. Using MDCK cells expressing RON as a model, a spindle-shape based screen was conducted, which identifies RSK2 among various intracellular proteins as a potential signaling molecule responsible for MSP-induced EMT. MSP stimulation dissociated RSK2 with Erk1/2 and promoted RSK2 nuclear translocation. MSP strongly induced RSK2 phosphorylation in a dose-dependent manner. These effects relied on RON and Erk1/2 phosphorylation, which is significantly potentiated by transforming growth factor (TGF)-β1, an EMT-inducing cytokine. Specific RSK inhibitor SL0101 completely prevented MSP-induced RSK phosphorylation, which results in inhibition of MSP-induced spindle-like morphology and suppression of cell migration associated with EMT. In HT-29 cancer cells that barely express RSK2, forced RSK2 expression results in EMT-like phenotype upon MSP stimulation. Moreover, specific siRNA-mediated silencing of RSK2 but not RSK1 in L3.6pl pancreatic cancer cells significantly inhibited MSP-induced EMT-like phenotype and cell migration.</p> <p>Conclusions</p> <p>MSP-induced RSK2 activation is a critical determinant linking RON signaling to cellular EMT program. Inhibition of RSK2 activity may provide a therapeutic opportunity for blocking RON-mediated cancer cell migration and subsequent invasion.</p

Preparation of FeO(OH) Modified with Polyethylene Glycol and Its Catalytic Activity on the Reduction of Nitrobenzene with Hydrazine Hydrate

Iron oxyhydroxide was prepared by dropping ammonia water to Fe(NO3)3.9H2O dispersed in polyethylene glycol (PEG) 1000. The catalyst was characterized by X-ray powder diffraction, Fourier transform infrared spectroscopy and laser particle size analyzer. The results showed the catalyst modified with polyethylene glycol was amorphous. The addition of PEG during the preparation make the particle size of the catalyst was smaller and more uniform. The catalytic performance was tested in the reduction of nitroarenes to corresponding amines with hydrazine hydrate, and the catalyst showed excellent activity and stability.