Capacity Lower Bounds of the Noncentral Chi-Channel with Applications to Soliton Amplitude Modulation

The channel law for amplitude-modulated solitons transmitted through a nonlinear optical fibre with ideal distributed amplification and a receiver based on the nonlinear Fourier transform is a noncentral chi-distribution with 2n degrees of freedom, where n = 2 and n = 3 correspond to the single- and dual-polarisation cases, respectively. In this paper, we study capacity lower bounds of this channel under an average power constraint in bits per channel use. We develop an asymptotic semi-analytic approximation for a capacity lower bound for arbitrary n and a Rayleigh input distribution. It is shown that this lower bound grows logarithmically with signal-to-noise ratio (SNR), independently of the value of n. Numerical results for other continuous input distributions are also provided. A half-Gaussian input distribution is shown to give larger rates than a Rayleigh input distribution for n = 1; 2; 3. At an SNR of 25 dB, the best lower bounds we developed are approximately 3:68 bit per channel use. The practically relevant case of amplitude shift-keying (ASK) constellations is also numerically analysed. For the same SNR of 25 dB, a 16- ASK constellation yields a rate of approximately 3:45 bit per channel use

A lower bound on the per soliton capacity of the nonlinear optical fibre channel

A closed-form expression for a lower bound on the per soliton capacity of the nonlinear optical fibre channel in the presence of (optical) amplifier spontaneous emission (ASE) noise is derived. This bound is based on a non-Gaussian conditional probability density function for the soliton amplitude jitter induced by the ASE noise and is proven to grow logarithmically as the signal-to-noise ratio increases

Leukemic stem cells activate lineage inappropriate signalling pathways to promote their growth

Acute Myeloid Leukemia (AML) is caused by multiple mutations which dysregulate growth and differentiation of myeloid cells. Cells adopt different gene regulatory networks specific to individual mutations, maintaining a rapidly proliferating blast cell population with fatal consequences for the patient if not treated. The most common treatment option is still chemotherapy which targets such cells. However, patients harbour a population of quiescent leukemic stem cells (LSCs) which can emerge from quiescence to trigger relapse after therapy. The processes that allow such cells to re-grow remain unknown. Here, we examine the well characterised t(8;21) AML sub-type as a model to address this question. Using four primary AML samples and a novel t(8;21) patient-derived xenograft model, we show that t(8;21) LSCs aberrantly activate the VEGF and IL-5 signalling pathways. Both pathways operate within a regulatory circuit consisting of the driver oncoprotein RUNX1::ETO and an AP-1/GATA2 axis allowing LSCs to re-enter the cell cycle while preserving self-renewal capacity