• Proceedings of the Korea Water Resources Association Conference
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• 2015.05a
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• pp.588-588
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• 2015

최근 기후변화로 인해 6 ~ 7년 주기로 가뭄의 정도가 점차 증가하고 있으며, 과잉취수로 인해 하천 상류 수원이 부족하여 지속적으로 하천 건천화가 발생되고 있는 실정이다. 물부족 지역의 경우 지하수와 같은 고갈되기 쉬운 물을 사용하므로 발생빈도가 높으며, 진행속도가 다른 자연재해와 달리 느리므로 시 공간적으로 정확하게 판단하기 어려워 해결이 장기화 되고 있다. 우리나라 물수급 지역이 급격하게 증감함에 따라 수량 확보와 탄력전인 하천수량 관리 기술이 사회적으로 중요시되고 있다. 이를 위한 수자원계획 도구로 여러 가지 방법이 제시되었다. 이러한 방법들 중 국내 실정에 맞도록 개선된 수자원평가계획모형인 K-WEAP(Korea-Water Evaluation And Planning System) 을 이용하여 물수지 분석하였다. 본 연구는 낙동강수계 금호강유역을 대상으로 중권역 내 행정구역별로 생활, 공업, 농업용수의 수요처와 공급량을 산정하고 이에 따른 네트워크를 구성하여 분석하였다. 각 하천의 자연유출량은 EPA(Environmental Protection Agency) 에서 개발한 강우-유출 모형인 SWMM(Storm Water Management Model) 에 의하여 산정된 결과를 적용하였다. 행정구역을 고려한 물수급 분석을 통해 물수급 전망이 세분화되어 있으나 실제 발생하는 물수급 평가의 어려움은 여전히 존재한다. 생공용수는 공급시설을 고려하여 물수급 분석을 수행하고, 농업용수는 월별로 수요량과 공급량을 검토하는 물수급 분석을 통해 국가수자원공급 계획을 반영한 광역, 기초자치단체의 수자원 확보 방안에 필요한 기초자료로 활용될 것이라 사료된다.

• Membrane Journal
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• v.29 no.3
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• pp.164-172
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• 2019

In this work, we demonstrate a facile process to prepare an electrolyte membrane for the supercapacitor based on a graft copolymer consisting of starch and poly(acrylonitrile) (PAN). The graft copolymer (starch-g-PAN) was synthesized via free radical polymerization initiated by ceric ions. The starch-g-PAN was dissolved in ionic liquid, i.e. 1-ethyl-3-methylimidazolium dicyanamide (EMIM DCA) without any organic solvents at room temperature. The gelation of polymer electrolyte membranes occurred by applying high temperature, i.e. $100^{\circ}C$ for 1 hour. The resultant electrolyte membrane was flexible and thus applied to flexible solid supercapacitors. The performance of the supercapacitor based on starch-g-PAN graft copolymer electrolyte reached 21 F/g at a current density of 0.5 A/g. The cell also showed high cyclic stability with 86% of retention rate within 10,000 cycles. The preparation of starch-g-PAN based polymer electrolyte membrane provides opportunities for facile fabrication of flexible solid supercapacitors with good performance.

• Research in Plant Disease
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• v.27 no.4
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• pp.137-148
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• 2021

Plant RNA viruses are one of the most destructive pathogens that cause a significant loss in crop production worldwide. They have evolved with high genetic diversity and adaptability due to the short replication cycle and high mutation rate during genome replication, which are characteristics of RNA viruses. Plant RNA viruses exist as quasispecies with high genetic diversity; thereby, a rapid population transition with new fitness can occur due to selective pressure resulting from environmental changes. Plant resistance can act as selective pressure and affect the fitness of the virus, which may lead to the emergence of resistance-breaking variants. In this paper, we introduced the evolutionary perspectives of plant RNA viruses and the driving forces in their evolution. Based on this, we discussed the mechanism of the emergence of variant viruses that overcome plant resistance. In addition, strategies for deploying plant resistance to viral diseases and improving resistance durability were discussed.

• Journal of Life Science
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• v.15 no.5 s.72
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• pp.726-733
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• 2005

Histone deacetylase (HDAC) inhibitors target key steps of tumor development. They inhibit proliferation, induce differentiation and/or apoptotic cell death, and exhibit potent antimetastatic and antiangiogenic properties in cancer cells in vitro and in vivo. Although they are emerging as a promising new treatment strategy in malignancy, how they exert their effect on human non-small cell lung cancer cells is as yet unclear. The present study was undertaken to investiate the underlying mechanism of a HDAC inhibitor trichostatin A (TSA)-induced growth arrest and its effect on the cell cycle control gene products in a human lung carcinoma cell line A549. TSA treaoent induced the growth inhibition and morphological changes in a concentration-dependent manner. Treatment of A549 cells with TSA resulted in a concentration-dependent increased G1 (under 100 ng/ml) and/or G2/M (200 ng/ml) cell population of the cell cycle as determined by flow cytometry Moreover, 200 ng/ml TSA treatment significantly induced the population of sub-G1 cells (23.0 fold of control). This anti-proliferative effect of TSA was accompanied by a marked inhibition of cyclins, positive regulators of cell cycle progression, and cyclin-dependent kinases (Cdks) expression and concomitant induction of tumor suppressor p53 and Cdk inhibitors such as p21 and p27 Although further studies are needed, these findings provide important insights into the possible molecular mechanisms of the anti-cancer activity of TSA in human lung carcinoma cells.

• Journal of Life Science
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• v.27 no.1
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• pp.78-88
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• 2017

Angiogenesis, the formation of new blood vessels, plays an important role in tumor growth and metastasis; therefore, it has become an important target in cancer therapy. Novel anticancer pharmaceutical products that have relatively few side effects or are non-cytotoxic must be developed, and such products may be obtained from traditional herbal medicines. Coptis chinensis Franch. is an herb used in traditional medicine for the treatment of inflammatory diseases and diabetes. However, potential antiangiogenic effects of C. chinensis water extract (CCFWE) have not yet been studied. The purpose of this study was to determine the antiangiogenic effect of CCFWE in order to evaluate its potential for an anticancer drug. We found that the treatment with CCFWE inhibited the major steps of the angiogenesis process, such as the endothelial cell proliferation, migration, invasion, and capillary-like tube formation in response to vascular endothelial growth factor (VEGF), and also resulted in the growth inhibition of new blood vessels in an ex vivo rat aortic ring assay. We also observed that CCFWE treatment arrested the cell cycle at the G0/G1 phase, preventing the G0/G1 to S phase cell cycle progression in response to VEGF. In addition, the treatment reduced the VEGF-induced activation of matrix metalloproteinases 2 and 9. Taken together, these findings indicate that CCFWE should be considered a potential anticancer therapy against pathological conditions where angiogenesis is stimulated during tumor development.

• Journal of Life Science
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• v.25 no.11
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• pp.1331-1337
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• 2015

S-allylcysteine (SAC) is an aged garlic derived water soluble organosulfur compound and has been suggested to have anticarcinogenic activity against diverse types of cancer cells. This review summarizes the cellular signaling pathways and molecular mechanisms whereby SAC exerts its effects on cellular proliferation, apoptosis, cell cycle progression and metastasis based on the results from both in vitro and in vivo studies. SAC activates proapoptotic proteins including Bax and caspase-3, but suppresses antiapoptotic Bcl-2 family proteins to bring about cancer cell death through mitochondria-mediated intrinsic pathway. SAC also inhibits cellular proliferation by inducing cell cycle arrest in which SAC reduces expression and activation of NF-κB, cyclins, Cdks, PCNA and c-Jun, but elevates expression of cell cycle inhibitor proteins p16 and p21 through suppression of both PI3K/Akt/mTOR and MAPK/ERK signaling pathways. And, SAC inhibits invasion and metastasis of cancer cells by inducing suppression of both angiogenesis and epithelial-mesenchymal transition (EMT) through decreased cyclooxygenase (COX)-2 expression and increased E-cadherin expression which were then caused by suppression of inhibitory transcription factors Id-1 and SLUG from SAC-mediated inactivation of both MAPK/ERK and PI3K/Akt/mTOR/NF-κB signaling pathways. Furthermore, SAC prevents toxic compound-induced carcinogenesis by inducing antioxidant enzymes such as glutathione-s-transferase (GST). Thus, SAC can be considered as a potential chemotherapeutic agent for the prevention and treatment of cancer.

• Journal of Life Science
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• v.25 no.1
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• pp.1-7
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• 2015

Cyclin D is a member of the cyclin protein family, which plays a critical role as a core member of the mammalian cell cycle machinery. D-type cyclins (D1, D2, and D3) bind to and activate the cyclin-dependent kinases 4 and 6, which can then phosphorylate the retinoblastoma tumor suppressor gene products. This phosphorylation in turn leads to release or derepression of E2F transcription factors that promote progression from the G1 to S phase of the cell cycle. Among the D-type cyclins, cyclin D3 encoded by the CCND3 gene is one of the least well studied. In the present study, we have investigated the biochemistry of the proteolytic mechanism that leads to loss of cyclin D3 protein. Treatment of human prostate carcinoma PC-3-M cells with lovastatin and actinomycin D resulted in a loss of cyclin D3 protein that was completely reversible by the peptide aldehyde calpain inhibitor, LLnL. Additionally, using inhibitors for various proteolytic systems, we show that degradation of cyclin D3 protein involves the $Ca^{2+}$-activated neutral protease calpain. Moreover, the half-life of cyclin D3 protein half-life increased by at least 10-fold in PC-3M cells in response to the calpain inhibitor. We have also demonstrated that the transient expression of the calpain inhibitor calpastatin increased cyclin D3 protein in serum-starved NIH 3T3 cells. These data suggested that the function of cyclin D3 is regulated by $Ca^{2+}$-dependent protease calpain.

• Journal of Life Science
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• v.17 no.7 s.87
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• pp.976-982
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• 2007

The purpose of this study was to determine the modulating effects of histone deacetylase inhibitor, trichostatin A, on the differentiation of mouse C2C12 myoblasts. We demonstrated that trichostatin A induced morphological changes of C2C12 myoblasts into smooth muscles and significantly increased the gene expression of smooth muscle markers including smooth muscle ${\alpha}-actin$ and transgelin. These results were due to the change in the expression level of cell cycle regulators in trichostatin A-treated C2C12 cells. Real-time PCR data revealed that cyclin dependent kinase inhibitor, p21, mRNA expression was significantly increased in trichostatin A-treated C2C12 cells. However, trichostaDn A rapidly decreased cyclin Dl mRNA expression necessary for cell cycle progression in 24hr after treatment. In conclusion, the strong inhibitory effects of trichostatin A on histone deacetylation induced transdifferentiation of C2C12 myoblasts into smooth muscle cells and these results are partly due to the changes in the expression of cell cycle regulators such as p21 and cyclin D1.

• Journal of Life Science
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• v.16 no.4
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• pp.589-597
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• 2006

Genistein, a natural isoflavonoid phytoestrogen, is a strong inhibitor of protein tyrosine kinase and DNA topoisomerase activities. There are several studies documenting molecular alterations leading to cell cycle arrest and induction of apoptosis by genistein as a chemopreventive agent in a variety of cancer cell lines; however, its mechanism of action and its molecular targets on human bladder carcinoma and leukemic cells remain unclear. In the present study, we have addressed the mechanism of action by which genistein suppressed the proliferation of T24 bladder carcinoma and U937 leukemic cells. Genistein significantly inhibited the cell growth and induced morphological changes, and induced the G2/M arrest of the cell cycle in both T24 and U937 cells with a relatively stronger cytotoxicity in U937. The G2/M arrest in T24 cells was associated with the inhibition of cyclin A, cyclin B1 and Cdc25C protein expression without alteration of tumor suppressor p53 and cyclin-dependent kinase (Cdk) inhibitor p21(WAF1/CIP1). However, the inhibitory effects of genistein on the cell growth of U937 cells were connected with a marked inhibition of cyclin B1 and an induction of Cdk inhibitor p21 proteins by p53-independent manner. These data suggest that genistein may exert a strong anticancer effect and additional studies will be needed to evaluate the different mechanisms between T24 and U937 cells.

• Journal of Life Science
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• v.16 no.4
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• pp.598-604
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• 2006

The $Ca^{2+}-activated$ neutral protease calpain induced proteolysis has been suggested to play a role in certain cell growth regulatory proteins. Cyclin proteolysis is essential for cell cycle progression. D-type cyclins, which form an assembly with cyclin-dependent kinases (cdk4 and cdk6), are synthesized earlier in G1 of the cell cycle and seem to be induced in response to external signals that promote entry into the cell cycle. Here we show that cyclin D3 protein levels are regulated at the posttranscriptional level by calpain protease. Treatment of human breast carcinoma MDA-MB-231 cells with lovastatin and actinomycin D resulted in a loss of cyclin D3 protein that was completely reversible by the peptide aldehyde calpain inhibitor, LLnL. The specific inhibitor of the 26S proteasome, lactacystin, the lysosome inhibitors, ammonium chloride and chloroquine, and the serine protease inhibitor, phenylmethylsulfonylfluoride (PMSF), did not block the degradation of cyclin D3 by lovastatin and actinomycin D. Results of in vitro degradation of cyclin D3 by purified calpain showed that cyclin D3 protein is degraded in a $Ca^{2+}-dependent$ manner, and the half-life of cyclin D3 protein was dramatically increased in LLnL treated cells. These data suggested that cyclin D3 protein is regulated by the $Ca^{2+}-activated$ protease calpain.