Some of the metal waste generated from KEPCO NF is being disposed of in the form of ingots. An ingot is a metal that is melted once and then poured into a mold to harden, and it is characterized by a uniform distribution of radioactive material. When measuring the uranium radioactivity in metal ingot with HPGe detector, 185.7 keV of U-235 is used typically because most gamma rays emitted at U-235 are distributed in low-energy regions below 200 keV. To analyze radioactivity concentration of U-235 with HPGe detector more accurately, self-attenuation due to geometrical differences between the calibration source and the sample must be corrected. In this study, the MCNP code was used to simulate the HPGe gamma spectroscopy system, and various processes were performed to prove the correlation with the actual values. First an metal ingottype standard source was manufactured for efficiency calibration, and the GEB coefficient was derived using Origin program. And through the comparison of actual measurements and simulations, the thickness of the detector’s dead layers were defined in all directions of Ge crystal. Additionally instead of making an metal ingot-type standard source every time, we analyzed the measurement tendency between commercially available HPGe calibration source (Marinelli beaker type) and the sample (metal ingot type), and derived the correction factor for geometry differences. Lastly the correction factor was taken into consideration when obtaining the uranium radioactivity concentration in the metal ingot with HPGe gamma spectroscopy. In conclusion, the U-235 radioactivity in metal ingot was underestimated about 25% of content due to the self-attenuation. Therefore it is reasonable to reflect this correction factor in the calculation of U-235 radioactivity concentration.

본 연구는 제경법을 이용한 유기초지 조성기술을 확립하기 위하여 2005년부터 2007년까지 3년 동안 수행하였으며 방목 축으로는 흑염소가 사용되었다. 시험설계는 관행조성구인 대조구, 퇴구비시용 후 방목구, 방목 후 퇴구비 시용구, 방목 후 퇴구비 시용 재방목구로 처리하였다. 목초정착률은 관행구인 대조구가 유기조성구에 비하여 현저하게 증가하였으며(p<0.05), 또한 건물생산성도 유기조성구에 비하여 대조구에서 현저한 증가를 나타냈다. 조성 후 연차가 경과

Patients with type II diabetes mellitus are more susceptible to colorectal cancer (CRC) incidence than non-diabetics. The anti-diabetic drug metformin is most commonly prescribed for the treatment of this disease and has recently shown antitumor effect in preclinical studies. The aberrant mutational activation in the components of RAS/RAF/MEK/ERK and PI3K/AKT/mTOR signaling pathway is very frequently observed in CRC. We previously reported that metformin inhibits the phosphorylation of ERK and BEZ235, a dual inhibitor of PI3K and mTOR, has anti-tumor activity against HCT15 CRC cells harboring mutations of KRAS and PIK3CA. Therefore, we hypothesized that simultaneous inhibition of two pathways by combining metformin with BEZ235 could be more effective in the suppression of proliferation than single agent treatment in HCT15 CRC cells. Here, we investigated the combinatory effect of metformin and BEZ235 on the cell survival in HCT15 CRC cells. Our study shows that both of the two signaling pathways can be blocked by this combinational strategy: metformin suppressed both pathways by inhibiting the phosphorylation of ERK, 4E-BP1 and S6, and BEZ235 suppressed PI3K/AKT/ mTOR pathway by reducing the phosphorylation of 4E-BP1 and S6. This combination treatment synergistically reduced cell viability. The combination index (CI) values ranged from 0.44 to 0.88, indicating synergism for the combination. These results offer a preclinical rationale for the potential therapeutic option for the treatment of CRC.

Molecular targeting for the altered signaling pathways has been proven to be effective for the treatment of many types of human cancer, including colorectal cancer (CRC). The dual phosphatidylinositol-3-kinase (PI3K) and mammalian target of rapamycin (mTOR) inhibitor BEZ235 has shown to exhibit potent antitumor activity against solid tumors. Autophagy is a cellular lysosomal catabolic process to maintain metabolic homeostasis, which has been known to be induced in response to many therapeutic agents in cancer cells. This process is negatively regulated by mTOR and often acts as prosurvival or prodeath mechanism following cancer therapeutics. The current study was designed to investigate the antiproliferation activity of BEZ235 and to evaluate the role of autophagy induced by BEZ235 using HCT15 CRC cells bearing ras oncogene mutation. We found that BEZ235 decreases cell viability, which was mostly dependent on G1 arrest of cell cycle via suppression of cyclin A expression. BEZ235 affects PI3K/Akt/mTOR signaling pathway by increasing the phosphorylation of AKT at Ser473 and RAS/RAF/MEK/ERK pathway by decreasing the phosphorylation of ERK at Tyr204. BEZ235 also stimulated autophagy induction as evidenced by the increased expression of LC3-II and abundant acidic vesicular organelles (AVOs) in the cytoplasm. In addition, the combination of BEZ235 with autophagy inhibitor chloroquine, a known antagonist of autophagy, counteracted the antiproliferation effect of BEZ235. Thus, our study indicates that autophagy induced in response to BEZ235 treatment appears to act as cell death mechanism in HCT15 CRC cells.