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GIS 공간분석 기반의 토석류피해지 토사유출 특성 연구
서준표(Seo, Junpyo),우충식(Woo, Choongshik),이창우(Lee, Changwoo),김동엽(Kim, Dongyeob) 한국방재학회 2018 한국방재학회논문집 Vol.18 No.5
산사태·토석류가 발생했을 때, 하류로 유출되는 토사량을 예측하는 것은 사방댐 규모·배치 등 사방사업에서 중요하다. 본 연구에서는 산사태·토석류 피해지역에 항공영상 촬영을 실시하고, GIS 공간분석을 수행하였다. 토석류 발생시 하류로 유출되는 토사량에는 계류길이, 계류폭, 발생원의 붕괴량이 영향을 미치는 것으로 나타났다. 하류로 유출되는 누적 토사량은 계류길이와 높은 상관관계로 나타났고, 이를 이용하여 토사유출량을 추정할 수 있는 식을 개발하였다. 개발된 식은 그룹화를 실시하고, 최종적으로 4가지 추정식을 제안하였다. 제안된 토석류 토사유출량 추정식은 토석류 발생시 하류로 유출되는 토사량을 예측하고, 사방댐 설계시 규모·배치 의사결정에 활용함으로써 재해예방 등 산지 하류지역의 방재효과에 기여할 수 있다. When landslides and debris flows occur, predicting sediment discharge is important for soil erosion control. In this study, aerial photography and GIS spatial analysis were carried out on a landslide and debris flow area. The sediment discharge was most affected by the flow length, flow width, and the amount of slope failure within the source area. In particular, the sediment discharge was highly correlated with the flow length. We have developed an equation that can estimate sediment discharge. The developed equations are grouped and four estimation equations are proposed. The developed sediment discharge equation can predict the amount of soil runoff downstream when a landslide and debris flow occur in a forest watershed. In addition, it can be used to make design decisions concerning the scale and location of erosion control dams, contributing to disaster prevention in downstream areas.
Lee, Jae Young,Seo, Dongyeob,You, Jiyeon,Chung, Sehee,Park, Jin Seok,Lee, Ji‐,Hyung,Jung, Su Myung,Lee, Youn Sook,Park, Seok Hee John Wiley and Sons Inc. 2017 FEBS letters Vol.591 No.3
<P>NOD‐like receptor family protein 3 (NLRP3)‐mediated inflammasome activation promotes caspase‐1‐dependent production of interleukin‐1β (IL‐1β) and requires the adaptor protein ASC. Compared with the priming and activation mechanisms of the inflammasome signaling pathway, post‐translational ubiquitination/deubiquitination mechanisms controlling inflammasome activation have not been clearly addressed. We here demonstrate that the deubiquitinating enzyme USP50 binds to the ASC protein and subsequently regulates the inflammasome signaling pathway by deubiquitinating the lysine 63‐linked polyubiquitination of ASC. USP50 knockdown in human THP‐1 cells and mouse bone marrow‐derived macrophages shows a significant decrease in procaspase‐1 cleavage, resulting in a reduced secretion of IL‐1β and interleukin‐18 (IL‐18) upon treatment with NLRP3 stimuli and a reduction in ASC speck formation and oligomerization. Thus, we elucidate a novel regulatory mechanism of the inflammasome signaling pathway mediated by the USP50 deubiquitinating enzyme.</P>
붕괴모의실험을 통한 산사태 조기경보용 계측센서의 반응성 분석 및 활용성 고찰
강민정,서준표,김동엽,이창우,우충식,Kang, Minjeng,Seo, Junpyo,Kim, Dongyeob,Lee, Changwoo,Woo, Choongshik 한국산림과학회 2019 한국산림과학회지 Vol.108 No.2
The goal of this study was to analyze the reactivity of a volumetric water content sensor (soil moisture sensor) and tensiometer and to review their use in the early detection of a shallow landslide. We attempted to demonstrate shallow and rapid slope collapses using three different soil ratios under artificial rainfall at 120 mm/h. Our results showed that the measured value of the volumetric water-content sensor converged to 30~37%, and that of the tensiometer reached -3~-5 kPa immediately before the collapse of the soil under all three conditions. Based on these results, we discussed a temporal range for early warnings of landslides using measurements of the volumetric water content sensors installed at the bottom of the soil slope, but could not generalize and clarify the exact timing for these early warnings. Further experiments under various conditions are needed to determine how to use both sensors for the early detection of shallow landslides. 이 연구는 붕괴모의실험을 통하여 체적함수비센서와 텐시오미터의 반응성을 분석하고, 산사태 조기경보용으로의 활용성을 검토하기 위해 수행되었다. 산림토양과 사질토의 배합비율을 조정한 3개의 토양조건에서 120 mm/h의 인공강우를 적용하여 얕은 깊이에서 빠르게 진행되는 붕괴형태를 실험적으로 모의하고, 그 과정에서의 두 센서의 반응을 분석하였다. 그 결과, 모든 실험조건에서 체적함수비센서 및 텐시오미터의 계측값은 각각 30~37%, -3~-5 kPa으로 수렴된 이후에 붕괴가 발생하였다. 실험결과를 토대로 토층 최하부에 설치된 체적함수비센서의 계측값을 활용하여 조기경보 발생시점의 범위를 논의하였으나, 이를 일반화하여 명확한 시점으로 규정할 수는 없었다. 두 센서를 실용적인 차원에서 산사태 조기경보용으로 활용하기 위해서는 다양한 조건에서의 추가적인 실험 및 검증이 필요할 것으로 생각되었다.
Lee Jaewon,Ha Jihoon,Kim Jun-Hyeong,Seo Dongyeob,Kim Minbeom,Lee Yerin,Park Seong Shil,Choi Dahee,Park Jin Seok,Lee Young Jae,Yang Siyoung,Yang Kyung-Min,Jung Su Myung,Hong Suntaek,Koo Seung-Hoi,Bae Y 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
The signaling pathways governing acetaminophen (APAP)-induced liver injury have been extensively studied. However, little is known about the ubiquitin-modifying enzymes needed for the regulation of APAP-induced liver injury. Here, we examined whether the Pellino3 protein, which has E3 ligase activity, is needed for APAP-induced liver injury and subsequently explored its molecular mechanism. Whole-body Peli3−/− knockout (KO) and adenovirus-mediated Peli3 knockdown (KD) mice showed reduced levels of centrilobular cell death, infiltration of immune cells, and biomarkers of liver injury, such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST), upon APAP treatment compared to wild-type (WT) mice. Peli3 deficiency in primary hepatocytes decreased mitochondrial and lysosomal damage and reduced the mitochondrial reactive oxygen species (ROS) levels. In addition, the levels of phosphorylation at serine 9 in the cytoplasm and mitochondrial translocation of GSK3β were decreased in primary hepatocytes obtained from Peli3−/− KO mice, and these reductions were accompanied by decreases in JNK phosphorylation and mitochondrial translocation. Pellino3 bound more strongly to GSK3β compared with JNK1 and JNK2 and induced the lysine 63 (K63)-mediated polyubiquitination of GSK3β. In rescue experiments, the ectopic expression of wild-type Pellino3 in Peli3−/− KO hepatocytes restored the mitochondrial translocation of GSK3β, but this restoration was not obtained with expression of a catalytically inactive mutant of Pellino3. These findings are the first to suggest a mechanistic link between Pellino3 and APAP-induced liver injury through the modulation of GSK3β polyubiquitination.
Lee, Ji-Hyung,Jung, Su Myung,Yang, Kyung-Min,Bae, Eunjin,Ahn, Sung Gwe,Park, Jin Seok,Seo, Dongyeob,Kim, Minbeom,Ha, Jihoon,Lee, Jaewon,Kim, Jun-Hyeong,Kim, Jun Hwan,Ooshima, Akira,Park, Jinah,Shin, D Nature Publishing Group 2017 NATURE CELL BIOLOGY Vol. No.
Although the ubiquitin-editing enzyme A20 is a key player in inflammation and autoimmunity, its role in cancer metastasis remains unknown. Here we show that A20 monoubiquitylates Snail1 at three lysine residues and thereby promotes metastasis of aggressive basal-like breast cancers. A20 is significantly upregulated in human basal-like breast cancers and its expression level is inversely correlated with metastasis-free patient survival. A20 facilitates TGF-β1-induced epithelial–mesenchymal transition (EMT) of breast cancer cells through multi-monoubiquitylation of Snail1. Monoubiquitylated Snail1 has reduced affinity for glycogen synthase kinase 3β (GSK3β), and is thus stabilized in the nucleus through decreased phosphorylation. Knockdown of A20 or overexpression of Snail1 with mutation of the monoubiquitylated lysine residues into arginine abolishes lung metastasis in mouse xenograft and orthotopic breast cancer models, indicating that A20 and monoubiquitylated Snail1 are required for metastasis. Our findings uncover an essential role of the A20–Snail1 axis in TGF-β1-induced EMT and metastasis of basal-like breast cancers.