Perturbation theory for localized solutions of sine-Gordon equation: decay of a breather and pinning by microresistor

We develop a perturbation theory that describes bound states of solitons localized in a confined area. External forces and influence of inhomogeneities are taken into account as perturbations to exact solutions of the sine-Gordon equation. We have investigated two special cases of fluxon trapped by a microresistor and decay of a breather under dissipation. Also, we have carried out numerical simulations with dissipative sine-Gordon equation and made comparison with the McLaughlin-Scott theory. Significant distinction between the McLaughlin-Scott calculation for a breather decay and our numerical result indicates that the history dependence of the breather evolution can not be neglected even for small damping parameter

Energy funneling in a bent chain of Morse oscillators with long-range coupling

A bent chain of coupled Morse oscillators with long-range dispersive interaction is considered. Moving localized excitations may be trapped in the bending region. Thus chain geometry acts like an impurity. An energy funneling effect is observed in the case of random initial conditions.Comment: 6 pages, 12 figures. Submitted to Physical Review E, Oct. 13, 200

Dark solitons in ferromagnetic chains with first- and second-neighbor interactions

We study the ferromagnetic spin chain with both first- and second-neighbor interactions. We obtained the condition for the appearance and stability of bright and dark solitons for arbitrary wave number inside the Brillouin zone. The influence of the second-neighbor interaction and the anisotropy on the soliton properties is considered. The scattering of dark solitons from point defects in the discrete spin chain is investigated numerically.Comment: 7 pages,5 figure

Confinement of discrete breathers in inhomogeneously profiled nonlinear chains

We investigate numerically the scattering of a moving discrete breather on a pair of junctions in a Fermi-Pasta-Ulam chain. These junctions delimit an extended region with different masses of the particles. We consider (i) a rectangular trap, (ii) a wedge shaped trap, and (iii) a smoothly varying convex or concave mass profile. All three cases lead to DB confinement, with the ease of trapping depending on the profile of the trap. We also study the collision and trapping of two DBs within the profile as a function of trap width, shape, and approach time at the two junctions. The latter controls whether one or both DBs are trapped

Withacnistin inhibits recruitment of STAT3 and STAT5 to growth factor and cytokine receptors and induces regression of breast tumours

BACKGROUND: The binding of STAT3 and STAT5 to growth factor and cytokine receptors such as EGFR and IL-6 receptor gp130 is critical to their activation and ability to contribute to malignant transformation. Therefore, interfering with these biochemical processes could lead to the discovery of novel anticancer agents. METHODS: Co-immunoprecipitation, western blotting, microscopy, DNA binding, invasion, and soft agar assays as well as a mouse model were used to investigate the mechanism by which the natural product Withacnistin (Wit) inhibits STAT 3/5 tyrosine phosphoryaltion and activation. RESULTS: Wit blocks EGF- and IL-6-stimulated binding of STAT3 and STAT5 to EGFR and gp130. Wit inhibits EGF-, PDGF-, IL-6-, IFNβ-, and GM-CSF-stimulation of tyrosine phosphorylation of STAT3 and STAT5 but not of EGFR or PDGFR. The inhibition of P-STAT3 and P-STAT5 occurred rapidly, within minutes of Wit treatment and growth factor stimulation. Wit also inhibits STAT3 nuclear translocation, DNA binding, promoter transcriptional activation, and it suppresses the expression levels of STAT3 target genes such as Bcl-xL and Mcl-1. Finally, Wit induces apoptosis, inhibits anchorage-dependent and -independent growth and invasion, and causes breast tumour regression in an ErbB2-driven transgenic mouse model. CONCLUSIONS: These data warrant further development of Wit as a novel anticancer drug for targeting tumours that harbour hyperactivated STAT3 and STAT5