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정영욱,Cheong, Young Wook,Thornton, Iain The Korean Society of Economic and Environmental G 1994 자원환경지질 Vol.27 No.1
강원도 상동지역의 옥동천 및 그 지류들을 대상으로 수질 파라메터(Eh-pH, 부유물질)의 측정과 하상퇴적물의 화학분석을 통하여 석탄광 및 금속 광산활동에 의한 옥동천의 수성 환경의 오염정도를 조사하였다. 옥동천의 조사유역을 상부와 하부 옥동천으로 구분할 때 상부 유역은 석탄광의 개발로 인한 황화물의 산화작용으로 인하여 수질은 매우 낮은 pH를 나타내 광산 산성수(Acid Mine Drainage)로 심하게 오염된 것으로 조사되었다. 또한 상부 옥동천에 용존된 철이 지류들의 유입과 하천의 aeration으로 철 산화물(floc)의 발생과 이의 침전으로 하천 바닥은 황갈색의 철산화물이 퇴적되어 있다. 그러나 상부 옥동천의 유속에 의해 일부 철 산화물이 침전되지 못한채 부유되어 옥동천은 매우 탁하게 보인다. 상부 옥동천온 천평천의 유입으로 인하여 낮은 pH의 산성수는 중화되지만 부유물질의 존재로 인하여 하부 옥동천은 계속 탁하여 광산 산성수의 영향이 지속되고 있다. sediment quality criteria와 비교해 볼 때 하부 옥동천의 하상퇴적물, 특히 상동 텅스텐-모리브덴늄 광미 저장댐과 인접된 지점의 하상퇴적물은 Pb, Cu, Zn, Co, Cd, As 및 Bi 등의 유해금속에 의해 농축되어 있어 퇴적물의 질이 상당히 악화되어 있다. 수중 및 저서 생물에 대한 서식처 및 수질을 개선하기 위해서 옥동천 상부에는 산성수를 중화시킬 수 있는 경제성 있는 수처리 장치의 도입과 중금속의 speciation의 연구가 필요할 것으로 사료된다. Geochemical investigations based on measurements of water parameters and sampling of stream sediments have been carried out, in the Okdongcheon stream and its tributaries in the Sangdong area of South Korea. There are two main problems occurring in the Okdongcheon stream: an acid mine drainage in the upper reaches and toxic trace metal contamination of the stream sediments mainly in the lower reaches. Acid mine water originating from coal mining was neutralized at the confluence of the Cheonpyongcheon stream whilst suspended solids due to flocculation of iron in water caused turbidity which was undesirable. Sediments in the Okdongcheon stream have been contaminated by mining activites. Iron was heavily concentrated in sediments in the upper Okdongcheon whilst toxic trace metals including Pb, Cu, Zn, Co, Cd, As and Bi were accumulated in sediments at stations draining metallic mining areas and near the tailings dam. There is now a requrement to neutralise the acid mine drainage and to use site-specific analysis of biological communities to ensure the conservation and preservation of aquatic organisms.
Yong, Wei Peng,Rha, Sun Young,Tan, Iain Bee-Huat,Choo, Su-Pin,Syn, Nicholas L.,Koh, Vivien,Tan, Shi-Hui,Asuncion, Bernadette Reyna,Sundar, Raghav,So, Jimmy Bok-Yan,Shabbir, Asim,Tan, Chee-Seng,Kim, Hy American Association for Cancer Research 2018 Clinical Cancer Research Vol.24 No.21
<P><B>Purpose:</B> The oxaliplatin plus S-1 and cisplatin plus S-1 regimens are interchangeably used in the management of advanced gastric cancer. The previously reported G-intestinal (G1) and G-diffuse (G2) intrinsic gene expression signatures showed promise for stratifying patients according to their tumor sensitivity to oxaliplatin or cisplatin.</P><P><B>Experimental Design:</B> The proof-of-concept, multicenter, open-label phase II “3G” trial was done to prospectively evaluate the feasibility and efficacy of using genomic classifiers to tailor treatment in gastric cancer. Patients’ tumors were classified as “G1” or “G2” using a nearest-prediction template method, or “G3” (unclear assignment) when FDR ≥ 0.05. The first 30 patients in the “G1” cohort were assigned oxaliplatin plus S-1 (SOX) chemotherapy; thereafter, subsequently recruited “G1” patients were treated with cisplatin plus S-1 (SP) chemotherapy. “G2” patients and “G3” patients were treated with SP and SOX chemotherapy, respectively.</P><P><B>Results:</B> A total of 48, 21, and 12 patients, respectively, were given “G1,” “G2,” and “G3” genomic assignments. Median turnaround time was 7 days (IQR, 5–9). Response rates were 44.8%, 8.3%, 26.7%, and 55.6% for the “G1-SOX,” “G1-SP,” “G2,” “G3” cohorts, respectively; and was higher in G1 patients treated with SOX compared with SP (<I>P</I> = 0.033). Exploratory analyses using the genomic classifier of Lei and colleagues validated the utility of the metabolic signature as a biomarker for predicting benefit from chemotherapy (log-rank <I>P</I> = 0.004 for PFS), whereas the Asian Cancer Research Group classifier did not demonstrate any predictive value.</P><P><B>Conclusions:</B> This bench-to-bedside effort establishes a reasonable turnaround time for gene expression profiling and possible utility of genomic classifiers in gastric cancer treatment stratification. <I>Clin Cancer Res; 24(21); 5272–81. ©2018 AACR</I>.</P>
Oncogenic Pathway Combinations Predict Clinical Prognosis in Gastric Cancer
Ooi, Chia Huey,Ivanova, Tatiana,Wu, Jeanie,Lee, Minghui,Tan, Iain Beehuat,Tao, Jiong,Ward, Lindsay,Koo, Jun Hao,Gopalakrishnan, Veena,Zhu, Yansong,Cheng, Lai Ling,Lee, Julian,Rha, Sun Young,Chung, Hyu Public Library of Science 2009 PLoS genetics Vol.5 No.10
<▼1><P>Many solid cancers are known to exhibit a high degree of heterogeneity in their deregulation of different oncogenic pathways. We sought to identify major oncogenic pathways in gastric cancer (GC) with significant relationships to patient survival. Using gene expression signatures, we devised an <I>in silico</I> strategy to map patterns of oncogenic pathway activation in 301 primary gastric cancers, the second highest cause of global cancer mortality. We identified three oncogenic pathways (proliferation/stem cell, NF-κB, and Wnt/β-catenin) deregulated in the majority (>70%) of gastric cancers. We functionally validated these pathway predictions in a panel of gastric cancer cell lines. Patient stratification by oncogenic pathway combinations showed reproducible and significant survival differences in multiple cohorts, suggesting that pathway interactions may play an important role in influencing disease behavior. Individual GCs can be successfully taxonomized by oncogenic pathway activity into biologically and clinically relevant subgroups. Predicting pathway activity by expression signatures thus permits the study of multiple cancer-related pathways interacting simultaneously in primary cancers, at a scale not currently achievable by other platforms.</P></▼1><▼2><P><B>Author Summary</B></P><P>Gastric cancer is the second leading cause of global cancer mortality. With current treatments, less than a quarter of patients survive longer than five years after surgery. Individual gastric cancers are highly disparate in their cellular characteristics and responses to standard chemotherapeutic drugs, making gastric cancer a complex disease. Pathway based approaches, rather than single gene studies, may help to unravel this complexity. Here, we make use of a computational approach to identify connections between molecular pathways and cancer profiles. In a large scale study of more than 300 patients, we identified subgroups of gastric cancers distinguishable by their patterns of driving molecular pathways. We show that these identified subgroups are clinically relevant in predicting survival duration and may prove useful in guiding the choice of targeted therapies designed to interfere with these molecular pathways. We also identified specific gastric cancer cell lines mirroring these pathway subgroups, which should facilitate the pre-clinical assessment of responses to targeted therapies in each subgroup.</P></▼2>
Fogelgren, Ben,Zuo, Xiaofeng,Buonato, Janine M.,Vasilyev, Aleksandr,Baek, Jeong-In,Choi, Soo Young,Chacon-Heszele, Maria F.,Palmyre, Auré,lien,Polgar, Noemi,Drummond, Iain,Park, Kwon Moo,Lazzara American Physiological Society 2014 American Journal of Physiology Vol.307 No.12
<P>Acute kidney injury is common and has a high mortality rate, and no effective treatment exists other than supportive care. Using cell culture models, we previously demonstrated that exocyst Sec10 overexpression reduced damage to renal tubule cells and speeded recovery and that the protective effect was mediated by higher basal levels of mitogen-activated protein kinase (MAPK) signaling. The exocyst, a highly-conserved eight-protein complex, is known for regulating protein trafficking. Here we show that the exocyst biochemically interacts with the epidermal growth factor receptor (EGFR), which is upstream of MAPK, and Sec10-overexpressing cells express greater levels of phosphorylated (active) ERK, the final step in the MAPK pathway, in response to EGF stimulation. EGFR endocytosis, which has been linked to activation of the MAPK pathway, increases in Sec10-overexpressing cells, and gefitinib, a specific EGFR inhibitor, and Dynasore, a dynamin inhibitor, both reduce EGFR endocytosis. In turn, inhibition of the MAPK pathway reduces ligand-mediated EGFR endocytosis, suggesting a potential feedback of elevated ERK activity on EGFR endocytosis. Gefitinib also decreases MAPK signaling in Sec10-overexpressing cells to levels seen in control cells and, demonstrating a causal role for EGFR, reverses the protective effect of Sec10 overexpression following cell injury in vitro. Finally, using an in vivo zebrafish model of acute kidney injury, morpholino-induced knockdown of <I>sec10</I> increases renal tubule cell susceptibility to injury. Taken together, these results suggest that the exocyst, acting through EGFR, endocytosis, and the MAPK pathway is a candidate therapeutic target for acute kidney injury.</P>