Interaction of edge waves with swell on a beach

Excitation of edge waves on a beach by incoming swell is considered on the basis of shallow-water model. Subharmonic resonance mechanism of interaction is analyzed by multi-scaled expansion asymptotic techniques. The generation of edge waves between wave breakers is found to have a dynamic threshold. It is defined by intensity and frequency of incoming swell, geometry of a shore zone. Nonlinear no stationary wave solutions for the envelope of interacting edge waves are described by generalized Sine-Gordon model. An infinite set of exact solutions are received by the Lamb method for the phase synchronism regime of wave’s interaction

Overall System Description and Safety Characteristics of Prototype Gen IV Sodium Cooled Fast Reactor in Korea

The Prototype Gen IV sodium cooled fast reactor (PGSFR) has been developed for the last 4 years, fulfilling the technology demonstration of the burning capability of transuranic elements included in light water reactor spent nuclear fuel. The PGSFR design has been focused on the robustness of safety systems by enhancing inherent safety characteristics of metal fuel and strengthening passive safety features using natural circulation and thermal expansion. The preliminary safety information document as a major outcome of the first design phase of PGSFR development was issued at the end of 2015. The project entered the second design phase at the beginning of 2016. This paper summarizes the overall structures, systems, and components of nuclear steam supply system and safety characteristics of the PGSFR. The research and development activities to demonstrate the safety performance are also briefly introduced in the paper

Correction: Dimethylfumarate Attenuates Renal Fibrosis via NF-E2-Related Factor 2-Mediated Inhibition of Transforming Growth Factor-β/Smad Signaling

TGF-β plays a key role in the development of renal fibrosis. Suppressing the TGF-β signaling pathway is a possible therapeutic approach for preventing this disease, and reports have suggested that Nrf2 protects against renal fibrosis by inhibiting TGF-β signaling. This study examines whether dimethylfumarate (DMF), which stimulates Nrf2, prevents renal fibrosis via the Nrf2-mediated suppression of TGF-β signaling. Results showed that DMF increased nuclear levels of Nrf2, and both DMF and adenovirus-mediated overexpression of Nrf2 (Ad-Nrf2) decreased PAI-1, alpha-smooth muscle actin (α-SMA), fibronectin and type 1 collagen expression in TGF-β-treated rat mesangial cells (RMCs) and renal fibroblast cells (NRK-49F). Additionally, DMF and Ad-Nrf2 repressed TGF-β-stimulated Smad3 activity by inhibiting Smad3 phosphorylation, which was restored by siRNA-mediated knockdown of Nrf2 expression. However, downregulation of the antioxidant response element (ARE)-driven Nrf2 target genes such as NQO1, HO-1 and glutathione S-transferase (GST) did not reverse the inhibitory effect of DMF on TGF-β-induced upregulation of profibrotic genes or extracellular matrix proteins, suggesting an ARE-independent anti-fibrotic activity of DMF. Finally, DMF suppressed unilateral ureteral obstruction (UUO)-induced renal fibrosis and α-SMA, fibronectin and type 1 collagen expression in the obstructed kidneys from UUO mice, along with increased and decreased expression of Nrf2 and phospho-Smad3, respectively. In summary, DMF attenuated renal fibrosis via the Nrf2-mediated inhibition of TGF-β/Smad3 signaling in an ARE-independent manner, suggesting that DMF could be used to treat renal fibrosis

DMF inhibits TGF-β-stimulated PAI-1, α-SMA, fibronectin and type 1 collagen expression.

<p>(A and B) Representative semi-quantitative RT-PCR analysis of the effects of DMF on PAI-1, α-SMA, fibronectin and type 1 collagen expression in TGF-β-stimulated NRK-49F cells. NRK-49F cells were starved for 12 h, treated with DMF for 1 h, and then stimulated with TGF-β (2 ng/ml) for 6 h (A) or 24 h (B). (C) Representative real-time RT-PCR analysis of the effects of DMF on TGF-β-stimulated PAI-1 and α-SMA mRNA expression. NRK-49F cells were treated with DMF for 1 h and then stimulated with TGF-β (2 ng/ml) for 6 h. Cells were harvested for real-time PCR analysis, and data represent the means ±SE of three independent measurements. ^*<i>P</i><0.01 vs. control; ^**<i>P</i><0.01, ^#<i>P</i><0.001 vs. TGF-β stimulation (upper panel); ^*<i>P</i><0.001 vs. control; ^**<i>P</i><0.01, ^#<i>P</i><0.001 vs. TGF-β stimulation (lower panel). (D and E) Representative Western blot analysis of the effect of DMF on PAI-1 expression in TGF-β-stimulated NRK-49F (D) and RMC (E) cells. Cells were starved for 12 h and pretreated with DMF for 1 h and then stimulated with TGF-β (2 ng/ml) for 12 h.</p

DMF inhibits the TGF-β/Smad3 signaling pathway.

<p>(A and B) Effects of DMF on TGF-β-stimulated PAI-1-Luc and (CAGA)₉MLP-Luc reporter constructs. AD-293 cells were transfected with PAI-1-Luc (A) or (CAGA)₉MLP-Luc (B) plasmids with or without ALK5, a constitutively active TGF-β type I receptor, for 24 h. Cells were starved for 12 h and stimulated with TGF-β (2 ng/ml) for 5 h. Data represent the means ±SEM of three independent measurements. (A) ^*<i>P</i><0.001 vs. reporter alone; ^**<i>P</i><0.001, ^***<i>P</i><0.01 vs. TGF-β stimulation (left panel). ^*<i>P</i><0.05 vs. reporter alone; ^**<i>P</i><0.01, ^***<i>P</i><0.05 vs. ALK5 stimulation (right panel). (B) ^*<i>P</i><0.01 vs. reporter alone; ^**<i>P</i><0.01 vs. TGF-β stimulation (left panel). ^*<i>P</i><0.01 vs. reporter alone; ^**<i>P</i><0.05, ^***<i>P</i><0.01 vs. ALK5 stimulation (right panel). (C and D) Representative Western blot analysis of the effect of DMF on TGF-β-stimulated Smad3 phosphorylation. Starved NRK-49F (C) and RMC (D) cells were pretreated with DMF for 1 h and then stimulated with TGF-β (2 ng/ml) for 1 h. Quantitative analysis of p-Smad3 to total Smad3 ratio. Data in bar graph are the mean ± SE of three independent measurements. (C) ^*<i>P</i><0.01 vs. control, ^**<i>P</i><0.05 vs. TGF-β stimulation. (D) ^*<i>P</i><0.001 vs. control, ^**<i>P</i><0.05, ^#<i>P</i><0.01, <i>^##P</i><0.001 vs. TGF-β stimulation.</p