Resonant radiation emitted by solitary waves via cascading in quadratic media.

We present a systematic investigation of the resonant radiation emitted by localized soliton-like wave-packets supported by second-harmonic generation in the cascading regime. We emphasize a general mechanism which allows for the resonant radiation to grow without the need for higher-order dispersion, primarily driven by the second-harmonic component, while radiation is also shed around the fundamental-frequency component through parametric down-conversion processes. The ubiquity of such a mechanism is revealed with reference to different localized waves such as bright solitons (both fundamental and second-order), Akhmediev breathers, and dark solitons. A simple phase matching condition is put forward to account for the frequencies radiated around such solitons, which agrees well with numerical simulations performed against changes of material parameters (say, phase mismatch, dispersion ratio). The results provide explicit understanding of the mechanism of soliton radiation in quadratic nonlinear media.

Quadratic Peregrine solitons resonantly radiating without higher-order dispersion.

We show that two-color Peregrine solitary waves in quadratic nonlinear media can resonantly radiate dispersive waves even in the absence of higher-order dispersion, owing to a phase-matching mechanism that involves the weaker second-harmonic component. We give very simple criteria for calculating the radiated frequencies in terms of material parameters, finding excellent agreement with numerical simulations.

Peptide DR8 suppresses epithelial-to-mesenchymal transition via the TGF-ß/MAPK signaling pathway in renal fibrosis.

AIMS: Renal fibrosis is a progressive disease that leads to renal dysfunction and end-stage renal failure, and there is currently no specific treatment. Our previous study showed that the 8-residue peptide DR8 (DHNNPQIR) exhibits potent antioxidant and antifibrotic properties, and accumulating evidence suggests that oxidative stress contributes greatly to fibrosis. The effects and mechanisms of DR8 on renal fibrosis remain unknown. MATERIALS AND METHODS: The effects of DR8 were assessed in a unilateral ureteral obstruction mouse model that received a daily, single-dose subcutaneous injection of 500 µg/kg DR8 for 14 days and in cultured cells (HK-2 and NIH-3T3 cells) treated with 5 ng/mL TGF-ß1 and 80 µM DR8. Western blotting, immunohistochemical staining, real-time qPCR and other tools were conducted to study the molecular mechanisms underlying antifibrotic effects. KEY FINDINGS: DR8 improved renal function and reduced injury and extracellular matrix (ECM) deposition. Inflammation and oxidative stress were alleviated by DR8 in vivo. DR8 also inhibited the activation of fibroblasts and ECM deposition in HK-2 and NIH-3T3 cells induced by TGF-ß1. In addition, epithelial-to-mesenchymal transition (EMT) was inhibited by DR8 both in vivo and in vitro. Mechanistic studies supported that DR8 inhibited ERK and p38 mitogen-activated protein kinase (MAPK) activation. These results indicate that DR8 attenuates renal fibrosis via suppression of EMT by antagonizing the MAPK pathway. SIGNIFICANCE: We provide mechanistic details for a potential therapeutic agent and establish a foundation for peptide therapeutics.

Protective effect of peptide DR8 on bleomycin-induced pulmonary fibrosis by regulating the TGF-ß/MAPK signaling pathway and oxidative stress.

Pulmonary fibrosis (PF) is a fatal and irreversible lung disease that eventually causes respiratory failure, lung dysfunction and death. The peptide DHNNPQIR-NH2 (DR8) has been reported to possess potent antioxidant activity, and an imbalance of oxidation/antioxidation is a crucial mechanism that causes PF. Here, we studied the ability of DR8 to improve PF and further explored the pathway in which DR8 plays a critical role. We found that after prophylactic or therapeutic treatment with DR8, fibrosis-associated indices, including marker proteins, proinflammatory cytokines and profibrogenic cytokines, were significantly downregulated. Importantly, DR8 could reduce bleomycin-induced pathological changes and collagen deposition, especially collagen I content. Furthermore, DR8 prominently upregulated nonenzymatic antioxidants and enzymatic antioxidants. Consistent with the in vivo results, we observed that DR8 significantly inhibited the proliferation and reactive oxygen species (ROS) generation of A549 cells and NIH3T3 cells stimulated with transforming growth factor-ß1 (TGF-ß1), as well as decreased NADPH oxidase 4 (NOX4) levels under the same conditions. Moreover, DR8 reversed the TGF-ß1-induced upregulation of phosphorylated ERK1/2 and p38 MAPK in cells and the bleomycin-induced upregulation of these indices in mice. Our results indicate that DR8 could prevent and treat PF by reducing oxidative damage and suppressing the TGF-ß/MAPK pathway. Because of the high efficiency and low toxicity of DR8, we consider that DR8 could be a candidate drug for PF, and our studies establish a foundation for the development of a lead compound to be used as a therapy for fibrosis-related diseases.

Super chirped rogue waves in optical fibers.

The super rogue wave dynamics in optical fibers are investigated within the framework of a generalized nonlinear Schrödinger equation containing group-velocity dispersion, Kerr and quintic nonlinearity, and self-steepening effect. In terms of the explicit rogue wave solutions up to the third order, we show that, for a rogue wave solution of order n, it can be shaped up as a single super rogue wave state with its peak amplitude 2n+1 times the background level, which results from the superposition of n(n+1)/2 Peregrine solitons. Particularly, we demonstrate that these super rogue waves involve a frequency chirp that is also localized in both time and space. The robustness of the super chirped rogue waves against white-noise perturbations as well as the possibility of generating them in a turbulent field is numerically confirmed, which anticipates their accessibility to experimental observation.

Rapeseed protein-derived antioxidant peptide RAP alleviates renal fibrosis through MAPK/NF-κB signaling pathways in diabetic nephropathy.

INTRODUCTION: Kidney fibrosis is the main pathologic change in diabetic nephropathy (DN), which is the major cause of end-stage renal disease. Current therapeutic strategies slow down but cannot reverse the progression of renal dysfunction in DN. Plant-derived bioactive peptides in foodstuffs are widely used in many fields because of their potential pharmaceutical and nutraceutical benefits. However, this type of peptide has not yet been studied in renal fibrosis of DN. Previous studies have indicated that the peptide YWDHNNPQIR (named RAP), a natural peptide derived from rapeseed protein, has an antioxidative stress effect. The oxidative stress is believed to be associated with DN. The aim of this study was to evaluate the pharmacologic effects of RAP against renal fibrosis of DN and high glucose (HG)-induced mesangial dysfunction. MATERIALS AND METHODS: Diabetes was induced by streptozotocin and high-fat diet in C57BL/6 mice and these mice were treated by subcutaneous injection of different doses of RAP (0.1 mg/kg and 0.5 mg/kg, every other day) or PBS for 12 weeks. Later, functional and histopathologic analyses were performed. Parallel experiments verifying the molecular mechanism by which RAP alleviates DN were carried out in HG-induced mesangial cells (MCs). RESULTS: RAP improved the renal function indices, including 24-h albuminuria, triglyceride, serum creatinine, and blood urea nitrogen levels, but did not lower blood glucose levels in DN mice. RAP also simultaneously attenuated extracellular matrix accumulation in DN mice and HG-induced MCs. Furthermore, RAP reduced HG-induced cell proliferation, but it showed no toxicity in MCs. Additionally, RAP inhibited the mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) signaling pathways. CONCLUSION: RAP can attenuate fibrosis in vivo and in vitro by antagonizing the MAPK and NF-κB pathways.