Nonlinear spectral management:linearization of the lossless fiber channel

Using the integrable nonlinear Schrodinger equation (NLSE) as a channel model, we describe the application of nonlinear spectral management for effective mitigation of all nonlinear distortions induced by the fiber Kerr effect. Our approach is a modification and substantial development of the so-called eigenvalue communication idea first presented in A. Hasegawa, T. Nyu, J. Lightwave Technol. 11, 395 (1993). The key feature of the nonlinear Fourier transform (inverse scattering transform) method is that for the NLSE, any input signal can be decomposed into the so-called scattering data (nonlinear spectrum), which evolve in a trivial manner, similar to the evolution of Fourier components in linear equations. We consider here a practically important weakly nonlinear transmission regime and propose a general method of the effective encoding/modulation of the nonlinear spectrum: The machinery of our approach is based on the recursive Fourier-type integration of the input profile and, thus, can be considered for electronic or all-optical implementations. We also present a novel concept of nonlinear spectral pre-compensation, or in other terms, an effective nonlinear spectral pre-equalization. The proposed general technique is then illustrated through particular analytical results available for the transmission of a segment of the orthogonal frequency division multiplexing (OFDM) formatted pattern, and through WDM input based on Gaussian pulses. Finally, the robustness of the method against the amplifier spontaneous emission is demonstrated, and the general numerical complexity of the nonlinear spectrum usage is discussed. © 2013 Optical Society of America.

Fibroblast growth factors:new insights, new targets in the management of diabetes

The fibroblast growth factor (FGF) family consists of 22 evolutionarily and structurally related proteins (FGF1 to FGF23; with FGF15 being the rodent ortholog of human FGF19). Based on their mechanism of action, FGFs can be categorized into intracrine, autocrine/paracrine and endocrine subgroups. Both autocrine/paracrine and endocrine FGFs are secreted from their cells of origin and exert their effects on target cells by binding to and activating specific single-pass transmembrane tyrosine kinase receptors (FGFRs). Moreover, FGF binding to FGFRs requires specific cofactors, namely heparin/heparan sulfate proteoglycans or Klothos for autocrine/paracrine and endocrine FGF signaling, respectively. FGFs are vital for embryonic development and mediate a broad spectrum of biological functions, ranging from cellular excitability to angiogenesis and tissue regeneration. Over the past decade certain FGFs (e.g. FGF1, FGF10, FGF15/FGF19 and FGF21) have been further recognized as regulators of energy homeostasis, metabolism and adipogenesis, constituting novel therapeutic targets for obesity and obesity-related cardiometabolic disease. Until recently, translational research has been mainly focused on FGF21, due to the pleiotropic, beneficial metabolic actions and the relatively benign safety profile of its engineered variants. However, increasing evidence regarding the role of additional FGFs in the regulation of metabolic homeostasis and recent developments regarding novel, engineered FGF variants have revitalized the research interest into the therapeutic potential of certain additional FGFs (e.g. FGF1 and FGF15/FGF19). This review presents a brief overview of the FGF family, describing the mode of action of the different FGFs subgroups, and focuses on FGF1 and FGF15/FGF19, which appear to also represent promising new targets for the treatment of obesity and type 2 diabetes.