Transverse modulational instability of partially incoherent soliton stripes

Based on the Wigner distribution approach, an analysis of the effect of partial incoherence on the transverse instability of soliton structures in nonlinear Kerr media is presented. It is explicitly shown, that for a Lorentzian incoherence spectrum the partial incoherence gives rise to a damping which counteracts, and tends to suppress, the transverse instability growth. However, the general picture is more complicated and it is shown that the effect of the partial incoherence depends crucially on the form of the incoherence spectrum. In fact, for spectra with finite rms-width, the partial incoherence may even increase both the growth rate and the range of unstable, transverse wave numbers.Comment: 5 pages, submitted to Phys. Rev.

New features of modulational instability of partially coherent light; importance of the incoherence spectrum

It is shown that the properties of the modulational instability of partially coherent waves propagating in a nonlinear Kerr medium depend crucially on the profile of the incoherent field spectrum. Under certain conditions, the incoherence may even enhance, rather than suppress, the instability. In particular, it is found that the range of modulationally unstable wave numbers does not necessarily decrease monotonously with increasing degree of incoherence and that the modulational instability may still exist even when long wavelength perturbations are stable.Comment: 4 pages, 2 figures, submitted to Phys. Rev. Let

Landau Damping and Coherent Structures in Narrow-Banded 1+1 Deep Water Gravity Waves

We study the nonlinear energy transfer around the peak of the spectrum of surface gravity waves by taking into account nonhomogeneous effects. In the narrow-banded approximation the kinetic equation resulting from a nonhomogeneous wave field is a Vlasov-Poisson type equation which includes at the same time the random version of the Benjamin-Feir instability and the Landau damping phenomenon. We analytically derive the values of the Phillips' constant $\alpha$ and the enhancement factor $\gamma$ for which the narrow-banded approximation of the JONSWAP spectrum is unstable. By performing numerical simulations of the nonlinear Schr\"{o}dinger equation we check the validity of the prediction of the related kinetic equation. We find that the effect of Landau damping is to suppress the formation of coherent structures. The problem of predicting freak waves is briefly discussed.Comment: 4 pages, 3 figure

Quasi-linear evolution of the modulational instability in the presence of partial incoherence

A basic system of model equations describing the quasi-linear development of the modulational instability in the presence of partial incoherence is derived. This system can be interpreted as balance equations for the number of quasi-particles in the Wigner spectrum where the basic processes which are active are emission and absorption of quasi-particles by quasi-particles with different wave vectors

The lysine specific demethylase-1 (LSD1/KDM1A) regulates VEGF-A expression in prostate cancer

Recurrent prostate cancer remains a major clinical challenge. The lysine specific demethylase-1 (LSD1/KDM1A), together with the JmjC domain-containing JMJD2A and JMJD2C proteins, have emerged as critical regulators of histone lysine methylation. The LSD1-JMJD2 complex functions as a transcriptional co-regulator of hormone activated androgen and estrogen receptors at specific gene promoters. LSD1 also regulates DNA methylation and p53 function. LSD1 is overexpressed in numerous cancers including prostate cancer through an unknown mechanism. We investigated expression of the LSD1 and JMJD2A in malignant human prostate specimens. We correlated LSD1 and JMJD2A expression with known mediators of prostate cancer progression: VEGF-A and cyclin A1. We show that elevated expression of LSD1, but not JMJD2A, correlates with prostate cancer recurrence and with increased VEGF-A expression. We show that functional depletion of LSD1 expression using siRNA in prostate cancer cells decreases VEGF-A and blocks androgen induced VEGF-A, PSA and Tmprss2 expression. We demonstrate that pharmacological inhibition of LSD1 reduces proliferation of both androgen dependent (LnCaP) and independent cell lines (LnCaP: C42, PC3). We show a direct mechanistic link between LSD1 overexpression and increased activity of pro-angiogenic pathways. New therapies targeting LSD1 activity should be useful in the treatment of hormone dependent and independent prostate cancer. (C) 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved