The domestic Pressurized Heavy Water Reactor (PWHR) nuclear power plant, Wolsong Unit 1, was permanently shut down on December 24, 2019. However, research on decommissioning has mainly focused on Pressurized Water Reactors (PWRs), with a notable absence of both domestic and international experience in the decommissioning of PHWRs. If proper business management such as radiation safety and waste is not performed, it can lead to increased business risks and costs in decommissioning. Therefore, the assessment of waste volume and cost, which provide fundamental data for the nuclear decommissioning process, is a crucial technical requirement before initiating the actual decommissioning of Wolsong Unit 1. Decommissioning radiation-contaminated structures and facilities presents significant challenges due to high radiation levels, making it difficult for workers to access these areas. Therefore, technology development should precede decommissioning process assessments and safety evaluations, facilitating the derivation of optimal decommissioning procedures and ensuring worker safety while enhancing the efficiency of decommissioning operations. In this study, we have developed a program to estimate decommissioning waste amounts for PHWRs, building upon prior research on PWR decommissioning projects while accounting for the specific design characteristics of PHWRs. To evaluate the amount of radioactive waste generated during decommissioning, we considered the characteristics of radioactive waste, disposal methods, packaging container specifications, and the criteria for the transfer of radioactive waste to disposal operators. Based on the derived algorithm, we conducted a detailed design and implemented the program. The proposed program is based on 3D modeling of the decommissioning components and the calculation of the Work Difficulty Factor (WDF), which is used to determine the time weighting factors for each task. Program users can select the cutting and packaging conditions for decommissioning components, estimate waste amount based on the chosen decommissioning method, and calculate costs using time weighting factors. It can be applied not only to PHWRs, but also to PWRs and non-nuclear fields, providing a flexible tool for optimizing decommissioning process.
After the major radioactivation structures (RPV, Core, SG, etc.) due to neutron irradiation from the nuclear fuel in the reactor are permanently shut down, numerous nuclides that emit alpha-rays, beta-rays, gamma-rays, etc. exist within the radioactive structures. In this study, nuclides were selected to evaluate the source term for worker exposure management (external exposure) at the time of decommissioning. The selection of nuclides was derived by sequentially considering the four steps. In the first stage, the classification of isotopes of major nuclides generated from the radiation of fission products, neutron-radiated products, coolant-induced corrosion products, and other impurities was considered as a step to select evaluation nuclides in major primary system structures. As a second step, in order to select the major radionuclides to be considered at the time of decommissioning, it is necessary to select the nuclides considering their half-life. Considering this, nuclides that were less than 5 years after permanent suspension were excluded. As a third step, since the purpose of reducing worker exposure during decommissioning is significant, nuclides that emit gamma rays when decaying were selected. As a final step, it is a material made by radiation from the fuel rod of the reactor and is often a fission product found in the event of a Severe accident at a nuclear power plant, and is excluded from the nuclide for evaluation at the time of decommissioning is excluded. The final selected Co-60 is a nuclide that emits high-energy gamma rays and was classified as a major nuclide that affects the reduction of radiation exposure to decommissioning workers. In the future, based on the nuclide selection results derived from this study, we plan to study the evaluation of worker radiation exposure from crud to decommissioning workers by deriving evaluation results of crud and radioactive source terms within the reactor core.
To date, there are no protocols optimized to the effective separation of spermatogonial stem cells (SSCs) from testicular cells derived from mouse testes, thus hindering studies based on mouse SSCs. In this study, we aimed to determine the most efficient purification method for the isolation of SSCs from mouse testes among previously described techniques. Isolation of SSCs from testicular cells derived from mouse testes was conducted using four different techniques: differential plating (DP), magnetic-activated cell sorting (MACS) post-DP, MACS, and positive and negative selection double MACS. DP was performed for 1, 2, 4, 8, or 16 h, and MACS was performed using EpCAM (MACSEpCAM), Thy1 (MACSThy1), or GFR α1 (MACSGFRα1) antibodies. The purification efficiency of each method was analyzed by measuring the percentage of cells that stained positively for alkaline phosphatase. DP for 8 h, MACSThy1 post-DP for 8 h, MACSGFRα1, positive selection double MACSGFRα1/EpCAM, and negative selection double MACSGFRα1/α-SMA were identified as the optimal protocols for isolation of SSCs from mouse testicular cells. Comparison of the purification efficiencies of the optimized isolation protocols showed that, numerically, the highest purification efficiency was obtained using MACSGFRα1. Overall, our results indicate that MACSGFRα1 is an appropriate purification technique for the isolation of SSCs from mouse testicular cells.
The purpose of this study was to identify the effects of cervical alignment, pain, and physique to apply proprioceptive neuromuscular facilitation( PNF) techniques in patients with forward head posture (FHP). The subjects of this study were 24 patients diagnosed with FHP. They were randomly divided into two groups: a PNF group(n=12) and a control group(n=12). The intervention was performed a total of 24 times, 30 min a day, six times a week for four weeks. Data on cervical alignment(forward head displacement, FHD), pain(visual analog scale, VAS), and physique(height, weight, and body mass index) were obtained pre- and post-intervention. Two-way repeated measures ANOVA was used to compare the groups and time. For FHD, the VAS, and physique(height and BMI), there was an interaction effect for the groups and time(p<.001, BMI: p<.05) and main effects for time(p<.001, BMI: p<.05). For weight, there were main effects of time(p<.01). For FHD(p<.01) and the VAS(p<.05), there were main effects for the groups. In the PNF group, there were significant improvements in FHD, VAS, and physique. In the control group, there was a significant increase in FHD. The results of this study indicated that PNF intervention using scapular and upper extremity patterns effective in FHP positively. The use of a therapeutic intervention on physique changes may also be effective in improving poor posture and help to better patients’ quality of life.
Graphene was grown on molybdenum (Mo) foil by a chemical vapor deposition method at different growth temperatures (1000°C, 1100°C, and 1200°C). The properties of graphene were investigated by X-ray diffraction (XRD), X-ray photoelectron spectroscopy, and Raman spectroscopy. The results showed that the quality of the deposited graphene layer was affected by the growth temperature. XRD results showed the presence of a carbide phase on the Mo surface; the presence of carbide was more intense at 1200°C. Additionally, a higher I2D/IG ratio (0.418) was observed at 1200°C, which implies that there are fewer graphene layers at this temperature. The lowest ID/IG ratio (0.908) for the graphene layers was obtained at 1200°C, suggesting that graphene had fewer defects at this temperature. The size of the graphene domains was also calculated. We found that by increasing the growth temperature, the graphene domain size also increased.
The purpose of this study is to develop a growth prediction model that can predict growth and development information influencing the production of citrus fruits: the growth model algorithm that can predict floral leaf ratio, number of fruit sets, fruit width, and overweight depending on the main period of growth and development with consideration of the applied weather factors. Every year, large scale of manpower was mobilized to investigate the production of outdoor-grown citrus fruits, but it was limited to recycling the data without an observation supporting system to systemize the database. This study intends to create a systematical database based on the basic data obtained through the observation supporting system in application of an algorithm according to the accumulated long term data and prepare a base for its continuous improvement and development. The importance of the observed data is increasingly recognized every year, and the citrus fruit observation supporting system is important for utilizing an effective policy and decision making according to various applications and analysis results through an interconnection and an integration of the investigated statistical data. The citrus fruit is a representative crop having a great ripple effect in Jeju agriculture. An early prediction of the growth and development information influencing the production of citrus fruits may be helpful for decision making in supply and demand control of agricultural products.
Pluripotent stem cells can be derived from both pre- and post-implantation embryos. Embryonic stem cells (ES cells), derived from inner cell mass (ICM) of blastocyst are naïve pluripotent and epiblast stem cells (EpiSCs) derived from post-implantation epiblast are primed pluripotent. The phenotypes and gene expression patterns of the two pluripotent stem cells are different each other and EpiSCs thought to be in a more advanced pluripotent (primed pluripotent state) than mouse ES cells (naïve pluripotent state). Therefore, we questioned whether EpiSCs are less potential to be differentiated into specialized cell types in vitro. EpiSCs were isolated from 5.5~6.5 day post coitum mouse embryos of the post-implantation epiblast. The EpiSCs could differentiate into all tree germ layers in vivo, and expressed pluripotency markers (Oct4, Nanog). Interestingly, EpiSCs also were able to efficiently differentiate into neural stem cells (NSCs). The NSCs differentiated from EpiSCs (EpiSC-NSCs) expressed NSC markers (Nestin, Sox2, and Musasi), self-renewed over passage 20, and could differentiate into two neural subtypes, neurons, astrocytes and oligodendrocytes. Next, we compared global gene expression patterns of EpiSC-NSCs with that of NSCs differentiated from ES cells and brain tissue. Gene expression pattern of brain tissue derived NSCs were closer to ES cell-derived NSCs than EpiSC-NSCs, indicating that the pluripotent stem cell-derived somatic cells could have different characteristics depending on the origin of pluripotent stem cell types. * This work was supported by the Next Generation Bio-Green 21 Program funded by the Rural Development Administration (Grant PJ 008009).
Neural stem cells (NSCs) are self-renewing tripotent cell populations and have capacity of neuronal (neurons) and glial (astrocytes and oligodendrocytes) differentiation. Many researchers have reported that NSCs have therapeutic effects in neurological disease by transplantation. However, it is not easy to obtain NSCs in vitro. Recently, Yamanaka and colleagues showed that somatic cells could be reprogrammed into pluripotent state by enforcing reprogramming factors. Induced pluripotent stem (iPS) cells undergo unlimited self-renewal and have differentiation potential into various types of cells like embryonic stem cells. Direct differentiation into a specialized cell types from iPS cells hold considerable promise for regenerative medicine as well as basic research. Here, we induced differentiation of iPS cells into NSCs in vitro and in vivo, which were compared with embryonic stem (ES) cell-derived NSCs and brain derived NSCs. NSCs from ES and iPS cells were morphologically indistinguishable from brain derived NSCs and stained positive for NSCs markers Nestin and Sox2. ES cells derived NSCs were transcriptionally distinguishable from brain derived NSCs. However, global gene expression pattern were similar but distinct between iPS derived NSCs and brain derived NSCs. Moreover, iPS derived NSCs were spontaneously aggregated upon passaging, formed ES cell like colonies, and finally reactivated Oct4-GFP. The spontaneously reverted GFP-positive cells (iPS-NSC-iPS) expressed similar levels of pluripotency markers (Oct4,Nanog) to ES and iPS cells, and could form germ line chimera. One possible explanation for this phenomenon is that spontaneously re-reprogramming was associated with transgene re-activation when iPS cells were differentiated into NSCs. However, NSCs from dox-inducible iPScells could not be reprogrammed into pluripotent state without doxycycline. Taken together, iPS derived NSCs were morphologically and similar to brain derived NSCs, but differ in gene expression pattern and maintenance. * This work was supported by the Next Generation Bio-Green21 Program funded by the Rural Development Administration (Grant PJ008009).
Cytokines are known to function as regulatory molecules that can be produced by virtually every nucleated cell type in the body, including lymphocytes, monocytes/macrophages, epithelial cells, fibroblasts, and many others. Cytokines include lymphocyte-derived factors (lymphokines), monocyte-derived factors (monokines), hematopoietic factors (colony-stimulating factors), connective tissue/ growth factors, and chemotactic chemokines. Cytokines released in response to infection can affect tumor development in different ways. When exposed to infectious agents, cytokines are secreted by sentinel cells, such as macrophages and dendritic cells. These cytokines include interleukin 1 (IL-1) and tumor necrosis factor-α, as well as others, such as IL-6, IL-12, and IL-18. When released in sufficient quantities, these molecules can cause inflammation. Chronic inflammation is highly associated with tumor initiation, promotion, and progression. In this article, we review the roles and mechanisms of cytokines in tumor development.
The objective of this study was to determine the effect of macrophages on growth of human colon cancer cells. The results showed that co-culture of colon cancer cells with macrophages inhibited the growth of colon cancer cells (HCT116 and SW620) depending on the number of macrophages, RAW 264.7 cells, and activated THP-1 cells accompanied by down regulation of pSTAT3 in cancer cells. We also found that expression and release of cancer cell growth inhibitory cytokines, IL-1 receptor antagonist (IL-1ra) and IL-10, was increased in macrophages. Blocking of the STAT3 pathway with specific inhibitor and siRNA of STAT3 abolished the growth of colon cancer cells and expression of IL-1ra and IL-10. In addition, neutralization of IL-1ra and IL-10 with antibodies resulted in reversal of macrophage-induced inhibition of cancer cell growth. These data showed that IL-1ra and IL-10 released from macrophages inhibit growth of colon cancer cells through inhibition of the STAT3 pathway.
This study was undertaken to evaluate the relationship between in vitro maturation and plasminogen activators (PAs) activity on porcine cumulus-oocytes complexes (COCs) exposed to oxidative stress. When COCs were cultured in maturation medium with hydrogen peroxide (H2O2), the proportion of the germinal vesicle breakdown (GVBD) and oocytes maturation were decreased with addition of H2O2, and were significantly (p<0.05) lower in medium with 0.1 mM H2O2 than control group. Also, the rate of degenerated oocytes was increased in as H2O2 concentration increased. When COCs were cultured for 48 h, three plasminogen-dependent lytic bands were observed: tissue-type PA (tPA); urokinase-type PA (uPA); and tPA-PA inhibitor (tPA-PAI). PA activity was quantified using SDS-PAGE and zymography. When H2O2 concentration was increased, tPA and tPA-PAI activities also increased in porcine oocytes cultured for 48 h, but not uPA. In other experiment, embryos were divided into three groups and cultured in (1) control medium, (2) control medium with 1.0 mM H2O2 and (3) control medium with 1.0 mM H2O2 along with catalase in concentrations of 0.01, 0.1, and 1.0 mg/ml, respectively. H2O2 decreased the rate of GVBD and maturation in porcine COCs but catalase revealed protective activity against oxidative stress caused by H2O2. In this experiment, tPA and tPA-PAI activities were higher in media with 1.0 mM H2O2 alone. Increasing concentration of catalase decreased tPA and tPA-PAI activities in porcine oocytes. These results indicate that the exposure of porcine follicular oocytes to ROS inhibits oocytes maturation to metaphase-II stage and increase the oocytes degeneration. Also, we speculated that increased ROS level may trigger tPA and tPA-PAI activities in porcine oocytes matured in vitro.
Chronic inflammatory diseases such as Crohn′s disease and ulcerative colitis are associated with increased risk of colon adenocarcinoma. Apoptic induction of colon cancer cells by cytokines and death receptors is an important anti-cancer therapy. We observed that co-administration of TNFα and IFNγ in human colon cancer cell line, HCT116, resulted in cell death and expression of IL-32. Cleavage forms of caspase-3, caspase-9, and PARP were increased in TNFα / IFNγ-treated HCT116. mRNA expression of death receptors, including TNFR1 and Fas were not changed and NO generation was not induced by combination of TNFα and IFNγ. However, mRNA expression of IL-32α, β, and γ was increased in TNFα / IFNγ-treated HCT116. To determine the effect of IL-32 in HCT116 cell apoptosis by TNFα / IFNγ stimulation, IL-32 siRNA-transfected HCT116 cells were cultured with TNFα / IFNγ and cell proliferation was measured. IL-32 siRNA induced slight recovery of cell viability of TNFα / IFNγ-stimulated HCT116. These results suggest that IL-32 is not directly related to apoptosis of HCT116 by TNFα / IFNγ stimulation. However, IL-32 expression by TNFα or TNFα / IFNγ in a colon cancer cell line is very interesting because of the unknown effect of IL-32 in colon cancer. Our study will contribute to development of studies for IL-32 function in human colon cancer and anti-cancer therapies using cytokines.
There are increasing interests in developing methods specifically detecting pathogenic Bursaphelenchus xylophilus. In order to develop a detecting method for B .xylophilus, at first we generated monoclonal antibodies (MAbs) specific to B. xylophilus, discriminating from other pine tree resident nematodes. Among 2304 hybridoma fusions screened. We finally selected a MAb clone, 9F10 and used for further study. To identify the antigenic target of MAb-9F10, we employed several biochemical methods such as SDS-PAGE, 2 dimensional electrophoresis, anion exchange chromatography, and immunoprecipitation to separate and isolate an antigenic target. Proteins from above methods were analyzed via nano-LC-ESI-Q-IT-MS. Peptides of GaLECtin were always detected from several proteomic analyses, suggesting that GaLECtin is the antigenic target of MAb-9F10.
The Maillard Reaction Products (MRPs) such as Glucose-tyrosine (Glu-Tyr) and Xylose-arginine (Xyl-Arg) have antioxidant, antimutagenic, and antibacterial effects. However, to date, still little is known about the other biological effects of the MRPs. In this study, we investigated whether the fructose-tyrosine MRP, 2,4-bis(p-hydroxyphenyl)-2-butenal (Fru-Tyr), could modulate cell cycle progression and NF-κB activity, and thereby induce apoptotic cell death of colon cancer cells. Treatment with different concentrations (10-40 μg/ ml) of Fru-Tyr for 24 h inhibited colon cancer cell (SW620 and HCT116) growth followed by induction of G2/M phase cell cycle arrest and apoptosis in a dose-dependent manner. We also found that Fru-Tyr suppressed tumor necrosis factor-alpha (TNF-α)-induced NF-κB transcriptional activity. Moreover, Fru-Tyr induced the expression of apoptotic gene, cleaved caspse-3. These results suggest that Fru-Tyr inhibited colon cancer cell growth through induction of G2/M phase cell cycle arrest and apoptotic cell death by modulating of NF-κB.