ESTABLISHMENT OF A MAINTENANCE PROGRAM TO PREVENT LOSS OF OFFSITE POWER IN NUCLEAR POWER PLANTS

Since the Fukushima accident in 2011, the importance of the electrical systems in nuclear power plants (NPPs) has been emphasized. The result has been that NPP regulators are enhancing their monitoring of loss of offsite power (LOOP) events. Korea Hydro & Nuclear Power Co. (KHNP) is reviewing the status and issues related to LOOPs, and is attempting to establish specific countermeasures to prevent LOOPs, because they can have severe consequences in the complicated maintenance schedule during an outage. A starting point for preventing LOOPs is the control of the loss of voltage (LOV)-initiating components. In order to reflect this in the risk assessment program, an LOV monitor is being developed for use during plant outages

Sargassum fulvellum

Ultraviolet (UV) radiation has been reported to induce cutaneous inflammation such as erythema and edema via induction of proinflammatory enzymes and mediators. Sargassum fulvellum is a brown alga of Sargassaceae family which has been demonstrated to exhibit antipyretic, analgesic, antiedema, antioxidant, antitumor, fibrinolytic, and hepatoprotective activities. The purpose of this study is to investigate anti-inflammatory effects of ethylacetate fraction of ethanol extract of Sargassum fulvellum (SFE-EtOAc) in HaCaT keratinocytes and BALB/c mice. In HaCaT cells, SFE-EtOAc effectively inhibited UVB-induced cytotoxicity (60 mJ/cm2) and the expression of proinflammatory proteins such as cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), and inducible nitric oxide synthase (iNOS). Furthermore, SFE-EtOAc significantly reduced UVB-induced production of proinflammatory mediators including prostaglandin E2 (PGE2) and nitric oxide (NO). In BALB/c mice, topical application of SFE-EtOAc prior to UVB irradiation (200 mJ/cm2) effectively suppressed the UVB-induced protein expression of COX-2, iNOS, and TNF-α and subsequently attenuated generation of PGE2 and NO as well. In another experiment, SFE-EtOAc pretreatment suppressed UVB-induced reactive oxygen species production and exhibited an antioxidant potential by upregulation of antioxidant enzymes such as catalase and Cu/Zn-superoxide dismutase in HaCaT cells. These results suggest that SFE-EtOAc could be an effective anti-inflammatory agent protecting against UVB irradiation-induced skin damages

Agmatine protects retinal ganglion cells from hypoxia-induced apoptosis in transformed rat retinal ganglion cell line

<p>Abstract</p> <p>Background</p> <p>Agmatine is an endogenous polyamine formed by the decarboxylation of L-arginine. We investigated the protective effects of agmatine against hypoxia-induced apoptosis of immortalized rat retinal ganglion cells (RGC-5). RGC-5 cells were cultured in a closed hypoxic chamber (5% O₂) with or without agmatine. Cell viability was determined by lactate dehydrogenase (LDH) assay and apoptosis was examined by annexin V and caspase-3 assays. Expression and phosphorylation of mitogen-activated protein kinases (MAPKs; JNK, ERK p44/42, and p38) and nuclear factor-kappa B (NF-κB) were investigated by Western immunoblot analysis. The effects of agmatine were compared to those of brain-derived neurotrophic factor (BDNF), a well-known protective neurotrophin for retinal ganglion cells.</p> <p>Results</p> <p>After 48 hours of hypoxic culture, the LDH assay showed 52.3% cell loss, which was reduced to 25.6% and 30.1% when agmatine and BDNF were administered, respectively. This observed cell loss was due to apoptotic cell death, as established by annexin V and caspase-3 assays. Although total expression of MAPKs and NF-κB was not influenced by hypoxic injury, phosphorylation of these two proteins was increased. Agmatine reduced phosphorylation of JNK and NF-κB, while BDNF suppressed phosphorylation of ERK and p38.</p> <p>Conclusion</p> <p>Our results show that agmatine has neuroprotective effects against hypoxia-induced retinal ganglion cell damage in RGC-5 cells and that its effects may act through the JNK and NF-κB signaling pathways. Our data suggest that agmatine may lead to a novel therapeutic strategy to reduce retinal ganglion cell injury related to hypoxia.</p

The Intestinal Copper Exporter CUA-1 Is Required for Systemic Copper Homeostasis in Caenorhabditis elegans

Copper plays key catalytic and regulatory roles in biochemical processes essential for normal growth, development, and health. Defects in copper metabolism cause Menkes and Wilson’s disease, myeloneuropathy, and cardiovascular disease and are associated with other pathophysiological states. Consequently, it is critical to understand the mechanisms by which organisms control the acquisition, distribution, and utilization of copper. The intestinal enterocyte is a key regulatory point for copper absorption into the body; however, the mechanisms by which intestinal cells transport copper to maintain organismal copper homeostasis are poorly understood. Here, we identify a mechanism by which organismal copper homeostasis is maintained by intestinal copper exporter trafficking that is coordinated with extraintestinal copper levels in Caenorhabditis elegans. Specifically, we show that CUA-1, the C. elegans homolog of ATP7A/B, localizes to lysosome-like organelles (gut granules) in the intestine under copper overload conditions for copper detoxification, whereas copper deficiency results in a redistribution of CUA-1 to basolateral membranes for copper efflux to peripheral tissues. Worms defective in gut granule biogenesis exhibit defects in copper sequestration and increased susceptibility to toxic copper levels. Interestingly, however, a splice isoform CUA-1.2 that lacks a portion of the N-terminal domain is targeted constitutively to the basolateral membrane irrespective of dietary copper concentration. Our studies establish that CUA-1 is a key intestinal copper exporter and that its trafficking is regulated to maintain systemic copper homeostasis. C. elegans could therefore be exploited as a whole-animal model system to study regulation of intra- and intercellular copper trafficking pathways

Strain-gradient-induced magnetic anisotropy in straight-stripe mixed-phase bismuth ferrites: An insight into flexomagnetic phenomenon

Implementation of antiferromagnetic compounds as active elements in spintronics has been hindered by their insensitive nature against external perturbations which causes difficulties in switching among different antiferromagnetic spin configurations. Electrically-controllable strain gradient can become a key parameter to tune the antiferromagnetic states of multiferroic materials. We have discovered a correlation between an electrically-written straight-stripe mixed-phase boundary and an in-plane antiferromagnetic spin axis in highly-elongated La-5%-doped BiFeO$_{3}$ thin films by performing polarization-dependent photoemission electron microscopy in conjunction with cluster model calculations. Model Hamiltonian calculation for the single-ion anisotropy including the spin-orbit interaction has been performed to figure out the physical origin of the link between the strain gradient present in the mixed phase area and its antiferromagnetic spin axis. Our findings enable estimation of the strain-gradient-induced magnetic anisotropy energy per Fe ion at around 5$\times$10$^{-12}$ eV m, and provide a new pathway towards an electric-field-induced 90$^{\circ}$ rotation of antiferromagnetic spin axis at room temperature by flexomagnetism.Comment: 32 pages, 5 figure

Multiplicity of positive solutions to a singular (p1,p2)(p_1,p_2)-Laplacian system with coupled integral boundary conditions

In this work, we investigate the existence and multiplicity results for positive solutions to a singular $(p_1,p_2)$-Laplacian system with coupled integral boundary conditions and a parameter $(\mu,\lambda) \in \mathbb{R}_+^3$. Using sub-super solutions method and fixed point index theorems, it is shown that there exists a continuous surface $\mathcal{C}$ which separates $\mathbb{R}_+^2 \times (0,\infty)$ into two regions $\mathcal{O}_1$ and $\mathcal{O}_2$ such that the problem under consideration has two positive solutions for $( \mu,\lambda) \in \mathcal{O}_1,$ at least one positive solution for $( \mu,\lambda) \in \mathcal{C}$, and no positive solutions for $( \mu,\lambda) \in \mathcal{O}_2.

Experimental approach to evaluate software reliability in hardware-software integrated environment

Reliability in safety-critical systems and equipment is of vital importance, so the probabilistic safety assessment (PSA) has been widely used for many years in the nuclear industry to address reliability in a quantitative manner. As many nuclear power plants (NPPs) become digitalized, evaluating the reliability of safety-critical software has become an emerging issue. Due to a lack of available methods, in many conventional PSA models only hardware reliability is addressed with the assumption that software reliability is perfect or very high compared to hardware reliability. This study focused on developing a new method of safety-critical software reliability quantification, derived from hardware-software integrated environment testing. Since the complexity of hardware and software interaction makes the possible number of test cases for exhaustive testing well beyond a practically achievable range, an importance-oriented testing method that assures the most efficient test coverage was developed. Application to the test of an actual NPP reactor protection system demonstrated the applicability of the developed method and provided insight into complex software-based system reliability. (C) 2020 Korean Nuclear Society, Published by Elsevier Korea LLC