The radiological characterization of SSCs (Structure, Systems and Components) plays one of the most important role for the decommissioning of KORI Unit-1 during the preparation periods. Generally, a regulatory body and laws relating to the decommissioning focus on the separation and appropriate disposal or storage of radiological waste including ILW (intermediate level waste), LLW (low level waste), VLLW (very low level waste) and CW (clearance waste), aligned with their contamination characteristics. The result of the preliminary radiological characterization of KORI Unit-1 indicated that, apart from neutron activated the RV (reactor vessel), RVI (reactor vessel internals), and BS (biological shielding concrete), the majorities of contamination were sorted to be less than LLW. Radiological contamination can be evaluated into two methods. Due to the difficulties of directly measuring contamination on the interior surfaces of the pipe, called CRUD, the assessment was implemented by modeling method, that is measuring contamination on the exterior surfaces of the pipes and calculating relative factors such as thickness and size. This indirect method may be affected by the surrounding radiation distribution, and only a few gamma nuclides can be measured. Therefore, it has limitation in terms of providing detailed nuclide information. Especially, α and β nuclides can only be estimated roughly by scaling factors, comparing their relative ratios with the existing gamma results. To overcome the limitation of indirect measurement, a destructive sampling method has been employed to assess the contamination of the systems and component. Samples are physically taken some parts of the systems or components and subsequently analyzed in the laboratory to evaluate detailed nuclides and total contamination. For the characterization of KORI Unit-1, we conducted the radiation measurement on the exterior surfaces of components using portable instruments (Eberline E-600 SPA3, Thermo G20-10, Thermo G10, Thermo FH40TG) at BR (boron recycle system) and SP (containment spray system) in primary system. Based on these results, the ProUCL program was employed to determine the destructive sample collection quantities based on statistical approach. The total of 5 and 8 destructive sample quantities were decided by program and successfully collected from the BR and SP systems, respectively. Samples were moved to laboratory and analyzed for the detail nuclide characteristics. The outcomes of this study are expected to serve as valuable information for estimating the types and quantities of radiological waste generated by decommissioning of KORI Unit-1.

Naturally occurring left ventricular hyperplasia is a rare but lethal disease. There are very few reports of this cardiac disease in captive nonhuman primates. In a colony of Macaca mulatta (Rhesus monkey) at California National Primate Research Center, a large number of rhesus macaques were diagnosed by autopsy with naturally occurring left ventricular hypertrophy without obvious underlying diseases over a 22-year period. The confirmatory diagnosis of ventricular hypertrophy was based on findings of notable left ventricular concentric hypertrophy with reduced left ventricular lumen, which is very similar to human ventricular hypertrophy cases. This report discusses an 11-year-old Macaca fascicularis monkey (Cynomolgus monkey, crab-eating macaque), weighing 2.95 kg, that was presented for enrollment in a pharmacokinetic (PK) study. During the PK experiment, the monkey died following a sudden decrease in percutaneous oxygen saturation and heart rate. Gross and histological examinations of the heart were performed. On gross pathology, the left ventricular wall was thickened, and the chamber lumen was reduced. In histopathological examination using hematoxylin- eosin and Masson-trichrome stains, fibrosis and myocyte disarray were not observed, but an increased cell density, compared to the normal heart, was confirmed. The autopsy results confirmed left ventricular hyperplasia as the major cause of death.

Osteoclasts originated from hematopoietic stem cells are multi-nucleated cells that can resorb the bone matrix. Receptor activator of nuclear factor kappa-B (RANK)/RANK ligand (RANKL) signaling pathway is crucial for the differentiation and activation of osteoclasts. In this study, we investigated for the first time whether or not RANKL induced mitogen- and stress-activated kinase 1 (MSK1) phosphorylation at Ser 376. Activation of MSK1 was detected as soon as 5 min after RANKL stimulation and sparsely detected at 30 min after stimulation. RANKL-induced MSK1 phosphorylation occurred in a dose-dependent manner. MSK1 is known as a downstream signaling molecule of cAMP-dependent protein kinase (PKA). Treatment with the PKA inhibitor H89 significantly suppressed c-Fos and nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1) induction upon RANKL stimulation. In addition, cAMP response element-binding protein (CREB) phosphorylation was extremely inhibited by H89 treatment. Mitogen-activated protein kinases (MAPKs) have been investigated for induction of MSK1 phosphorylation. Specific signaling pathway inhibitors for p38 and extracellular signal-regulated kinases (ERKs) significantly blocked RANKL-induced MSK1 activation. Finally, as a downstream effector of the p38-MSK1 pathway, c-Fos transcriptional activity was determined. RANKL-mediated elevation of c-Fos transcriptional activity was significantly suppressed by p38 inhibitor. Moreover, a dominant negative form of CREB suppressed activation of NFATc1. In conclusion, RANKL-stimulated MSK1 phosphorylation could play a role in induction of NFATc1 through CREB and c-Fos activation as a downstream molecule of p38, ERK MAPKs, and PKA. Our results support basic information for the development of osteoclast specific inhibitors.