X-ray Diagnosis of Amoebic Liver Abscesses with a Radiopaque Meidum

Kim, Sung Dae,Lieske, H,Haage, H.,Buck, A.A. 부산의대 1966 부산의대잡지 - 부산대학교 의과대학 Vol.6 No.1

Underspecified Japanese Semantics in a Machine Translation System

( Bjorn Gamback ),( Christian Lieske ),( Yoshiki Mori ) 한국언어정보학회 1996 국제 워크샵 Vol.1996 No.-

Semantic representations which are unerspecified with respect to, for example, scope, have recently attracted much attention. Most research in this area has focused on treating English language phenomena in a theoretical fashion. Our paper deviates from this twofold: We take Japanese as the language of our in-vestigations and describe how our ideas about underspecified Japanese semantics (e.g., on modality adverbs) have been implemented in a spoken-language machine translation system.

1,2,3,4,6-penta-O-galloyl-beta-d-glucose attenuates renal cell migration, hyaluronan expression, and crystal adhesion

Lee, J.H.,Yehl, M.,Ahn, K.S.,Kim, S.H.,Lieske, J.C. North-Holland ; Elsevier Science Ltd 2009 european journal of pharmacology Vol.606 No.1

Calcium oxalate monohydrate (COM) crystals bind avidly to the surface of proliferating and migrating renal endothelial cells, and oxalate-induced peroxidative injury can promote crystal attachment to renal epithelial cells. 1,2,3,4,6-penta-O-galloyl-beta-d-glucose (PGG), isolated from a traditional herbal remedy, inhibits vascular endothelial growth factor (VEGF) stimulated proliferation and migration of human umbilical vein endothelial cells (HUVECs) and has antioxidant activity. This study was performed to determine if PGG altered calcium oxalate monohydrate (COM) crystal adhesion to cells, perhaps via a change in cell surface properties. PGG significantly decreased COM crystal adhesion to cultured MDCK I cells at a low concentration (<10 μM) which was not cytotoxic. PGG exerted anti-adhesion effects whether cells or crystals were pre-coated. PGG also inhibited cell migration after scrape-wounding, decreased subsequent adhesion of crystals to proliferating and migrating cells, and decreased expression of the crystal binding molecule hyaluronan. These findings suggest that PGG represents a potential urolithiasis prevention compound. Anti-crystal adhesion effects appear multifaceted involving crystal coating by PGG, as well as decreased cell migration and the associated surface expression of hyaluronan. The latter represents a novel mechanism of nephrolithiasis prevention.

Decursin Prevents Cisplatin-Induced Apoptosis <i>via</i> the Enhancement of Antioxidant Enzymes in Human Renal Epithelial Cells

Kim, Jeong Hwan,Jeong, Soo-Jin,Kwon, Hee-Young,Park, Sang Yoon,Lee, Hyo-Jung,Lee, Hyo-Jeong,Lieske, John Charles,Kim, Sung-Hoon Pharmaceutical Society of Japan 2010 Biological & pharmaceutical bulletin Vol.33 No.8

<P>Adverse effects, nephrotoxicity and hepatotoxicity, of anticancer drugs such as cisplatin have limited the usage for cancer therapy. Therefore, development or identification of supplement agents in anticancer drugs is attractive to reduce side effects and enhance antitumor activity. Here, we found that decursin isolated from <I>Angelica gigas</I> showed protective effects of cisplatin-induced damage in normal human primary renal epithelial cells (HRCs). We found that decursin significantly blocked cisplatin-induced cytotoxicity by 2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2<I>H</I>-tetrazolium-5-carboxanilide (XTT) assay in HRCs. Further, we found that decursin inhibited sub-G1 and cell death by suppression of cleavage of caspase-3, -9 and poly(ADP-ribose) polymerase (PARP) induced by cisplatin treatment in HRCs. Importantly, decursin effectively restored the activities of Cu/Zn superoxide dismutase (SOD), catalase and glutathione peroxidase in cisplatin-treated HRCs. Taken together, our findings demonstrate that decurcin prevents cisplatin-induced cytotoxicity and apoptosis through the activation of antioxidant enzymes in HRCs and suggest further that combination of decursin might suppressed adverse effects of anticancer drugs in cancer patients.</P>

Gallotannin Suppresses Calcium Oxalate Crystal Binding and Oxalate-Induced Oxidative Stress in Renal Epithelial Cells

Lee, Hyo-Jung,Jeong, Soo-Jin,Park, Moon Nyeo,Linnes, Michael,Han, Hee Jeoung,Kim, Jin Hyoung,Lieske, John Charles,Kim, Sung-Hoon Pharmaceutical Society of Japan 2012 Biological & pharmaceutical bulletin Vol.35 No.4

<P>Calcium oxalate monohydrate (COM) crystals bind avidly to the surface of proliferating and migrating renal endothelial cells, perhaps a key event in kidney stone formation. Oxalate-induced pre-oxidative stress can further promote crystal attachment cells. Natural products including gallotannins found in green teas have been studied as potentially novel treatments to prevent crystal retention and kidney stone formation. Gallotannin significantly inhibited COM crystal growth and binding to Madin-Darby Canine Kidney Cells type I (MDCK I) renal epithelial cells at non-toxic concentrations. Reverse transcription polymerase chain reaction (RT-PCR) analysis revealed that gallotannin significantly attenuated oxalate-induced mRNA and protein expressions of monocyte chemoattractant protein 1 (MCP-1), osteopontin (OPN), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit p22<SUP>phox</SUP> and p47<SUP>phox</SUP> in human primary renal epithelial cells (HRCs). Gallotannin also reduced the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) as well as enhanced antioxidant enzyme superoxide dismutase (SOD) activity in oxalate treated HRCs. Taken together, our findings suggest that gallotannin can contribute to nephrolithiasis prevention <I>via</I> direct effects on renal epithelial cells including suppression of COM binding and MCP-1 and OPN expression, along with augmenting antioxidant activity.</P>

1,2,3,4,6-Penta-O-galloyl-beta-D-glucose reduces renal crystallization and oxidative stress in a hyperoxaluric rat model

Lee, Hyo-Jung,Jeong, Soo-Jin,Lee, Hyo-Jeong,Lee, Eun-Ok,Bae, Hyunsu,Lieske, John C,Kim, Sung-Hoon International Society of Nephrology 2011 Kidney international Vol.79 No.5

Adhesion of calcium oxalate (CaOx) crystals to kidney cells may be a key event in the pathogenesis of kidney stones associated with marked hyperoxaluria. Previously, we found that 1,2,3,4,6-penta-O-galloyl-β-D-glucose (PGG), isolated from a traditional medicinal herb, reduced CaOx crystal adhesion to renal epithelial cells by acting on the cells as well as on the crystal surface. Here we used the ethylene glycol (EG)-mediated hyperoxaluric rat model and found evidence of oxidant stress as indicated by decreases in the activities of the renal antioxidant enzymes, superoxide dismutase, catalase, and glutathione peroxidase, with increased kidney cell apoptosis and serum malondialdehyde levels, all evident by 21 days of EG treatment. These effects of hyperoxaluria were reversed by concurrent PGG treatment along with decreased urinary oxalate levels and CaOx supersaturation. Renal epithelial cell expression of the crystal binding molecule hyaluronan increased diffusely within 7 days of EG initiation, suggesting it is not a result of but precedes crystal deposition. Renal cell osteopontin (OPN) was also upregulated in EG-treated animals, and PGG significantly attenuated overexpression of both OPN and hyaluronan. Thus, our findings demonstrate that PGG reduces renal crystallization and oxidative renal cell injury, and may be a candidate chemopreventive agent for nephrolithiasis.

<i>Rhus verniciflua</i> Stokes prevents cisplatin-induced cytotoxicity and reactive oxygen species production in MDCK-I renal cells and intact mice

Lee, Joo-Ho,Lee, Hyo-Jung,Lee, Hyo-Jeong,Choi, Won-Cheol,Yoon, Seong-Woo,Ko, Seong-Gyu,Ahn, Kwang Seok,Choi, Seung-Hoon,Ahn, Kyoo-Seok,Lieske, John C.,Kim, Sung-Hoon Elsevier 2009 Phytomedicine Vol.16 No.2

<P><B>Abstract</B></P><P>Cisplatin-induced oxidative stress can cause liver and kidney damage, thus limiting therapeutic efficacy. Thus, in the present study, since <I>Rhus verniciflua</I> Stokes (RVS) containing flavonoids has antioxidant effects, we investigated whether it can protect cisplatin-induced toxicity <I>in vitro</I> and <I>in vivo</I>, The <I>in vitro</I> effects of RVS on the cell viability and reactive oxygen species (ROS) production were investigated using cisplatin-treated Madin–Darby Canine kidney (MDCK)-I renal cells. Its <I>in vivo</I> effects were also studied in BALB/c mice inoculated with CT-26 colon adenocarcinoma cells and treated with cisplatin with or without RVS. Liver and renal functions were assessed together with indices of tissue oxidation. RVS prevented cisplatin-induced cytotoxicity and ROS release against MDCK-I cells. RVS alone exerted modest antitumor activity against CT-26 cells. When used concurrently with cisplatin, RVS prevented the increases in serum blood urea nitrogen (BUN), creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and NO, while reducing liver and kidney tissue MDA content, and increasing catalase, glutathione (GSH), and superoxide dismutase (SOD) activities. Moreover, the antitumor efficacy of cisplatin was not altered by concurrent administration of RVS. These findings demonstrate that RVS prevents cisplatin-induced toxicity <I>in vitro</I> and <I>in vivo</I> via an antioxidant activity without hurting its antitumor effectiveness, suggesting that RVS can be usefully applied to the neoplastic patients as a combined chemopreventive agent with cisplatin.</P>