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( Yu Lan Cui ),황현숙 ( Hyun Suk Hwang ),신성현 ( Seong Hyun Shin ),서용철 ( Yong Cheol Suh ),김창수 ( Chang Soo Kim ) 한국지리정보학회 2008 한국지리정보학회지 Vol.11 No.3
The control points are important assets of countries which express the most accurate location information that is used in surveying land and other measurements. The location information has played an important role in our daily lives with the development of ubiquitous technology. While many researchers have recently applied new technology like RFID(Radio-Frequency Identification) to the effective management of control points, the research into data retrieval and the interoperability of control point data is still primitive step. Therefore, we construct a data modeling to effectively manage control points using ontology data structure and focus on semantic retrieval method. Our retrieval system can provide the inferred and associated information among data using Protege-OWL tool. Our system has advantages in reducing the number of repeated queries by hierarchy searching and improving the searching time by association searching. Also, we propose an effective method to construct retrieval systems being able to edit items of categories and properties without editing the related codes.
Nicotine exacerbates tacrolimus-induced renal injury by programmed cell death
( Yu Ji Jiang ),( Sheng Cui ),( Kang Luo ),( Jun Ding ),( Qi Yan Nan ),( Shang Guo Piao ),( Mei Ying Xuan ),( Hai Lan Zheng ),( Yong Jie Jin ),( Ji Zhe Jin ),( Jung Pyo Lee ),( Byung Ha Chung ),( Bum 대한내과학회 2021 The Korean Journal of Internal Medicine Vol.36 No.6
Background/Aims: Cigarette smoking is an important modifiable risk factor in kidney disease progression. However, the underlying mechanisms for this are lacking. This study aimed to assess whether nicotine (NIC), a major toxic component of cigarette smoking, would exacerbates tacrolimus (TAC)-induced renal in-jury. Methods: Sprague-Dawley rats were treated daily with NIC, TAC, or both drugs for 4 weeks. The influence of NIC on TAC-caused renal injury was examined via renal function, histopathology, oxidative stress, mitochondria, endoplasmic reticulum (ER) stress, and programmed cell death (apoptosis and autophagy). Results: Both NIC and TAC significantly impaired renal function and histopathology, while combined NIC and TAC treatment aggravated these parameters beyond the effects of either alone. Increased oxidative stress, ER stress, mitochondrial dysfunction, proinflammatory and profibrotic cytokine expressions, and programmed cell death from either NIC or TAC were also aggravated by the two combined. Conclusions: Our observations suggest that NIC exacerbates chronic TAC nephrotoxicity, implying that smoking cessation may be beneficial for transplant smokers taking TAC.
Lan Hong,Guo-Hua Gong,Li Yu,Ming-Xia Song,Xun Cui,Zhe-Shan Quan 대한약학회 2013 Archives of Pharmacal Research Vol.36 No.11
A series of 7-alkoxy-4,5-dihydro-[1,2,4]oxadiazolo[4,3-a]quinolin-1-ones was synthesized and theirnegative inotropic effects were evaluated by measuring theleft atrium stroke volume in isolated rabbit heart preparations. All compounds moderated the cardiac workload bydecreasing heart rate and contractility (inotropic effects). Among them, compound 6 was found to be best potent witha -28.89 ± 1.91 % decrease in the stroke volume at aconcentration of 3 9 10-5 M in our in vitro study.
Lan, Hai-Nan,Jiang, Hai-Long,Li, Wei,Wu, Tian-Cheng,Hong, Pan,Li, Yu Meng,Zhang, Hui,Cui, Huan-Zhong,Zheng, Xin Asian Australasian Association of Animal Productio 2015 Animal Bioscience Vol.28 No.4
B-32 is one of a panel of monoclonal anti-idiotypic antibodies to growth hormone (GH) that we developed. To characterize and identify its potential role as a novel growth hormone receptor (GHR) agonist, we determined that B-32 behaved as a typical $Ab2{\beta}$ based on a series of enzyme-linked immunosorbent assay assays. The results of fluorescence-activated cell sorting, indirect immunofluorescence and competitive receptor binding assays demonstrated that B-32 specifically binds to the GHR expressed on target cells. Next, we examined the resulting signal transduction pathways triggered by this antibody in primary porcine hepatocytes. We found that B-32 can activate the GHR and Janus kinase (2)/signal transducers and activators of transcription (JAK2/STAT5) signalling pathways. The phosphorylation kinetics of JAK2/STAT5 induced by either GH or B-32 were analysed in dose-response and time course experiments. In addition, B32 could also stimulate porcine hepatocytes to secrete insulin-like growth factors-1. Our work indicates that a monoclonal anti-idiotypic antibody to GH (B-32) can serve as a GHR agonist or GH mimic and has application potential in domestic animal (pig) production.
Cui, Xiang‐,Dan,Lee, Mi‐,Jin,Kim, Jong‐,Hyun,Hao, Pei‐,Pei,Liu, Lan,Yu, Goung‐,Ran,Kim, Dae‐,Ghon Wiley Subscription Services, Inc., A Wiley Company 2013 Hepatology Vol.57 No.6
<P><B>Abstract</B></P><P>Eph receptor 2 (EphA2) overexpression is frequently accompanied by the loss of its cognate ligand during tumor progression. However, the molecular mechanism of this ligand‐independent promotion of tumor by EphA2 remains unclear in highly malignant and fatal cholangiocarcinoma (CC). We examined the biological role of EphA2 in tumor growth and metastasis in CC tissues and cells according to the degree of differentiation and we explored the downstream signaling pathways of EphA2. Growth factor‐mediated EphA2 overexpression itself leads to the activation of the mammalian target of rapamycin complex 1 (mTORC1) and extracellular signal‐regulated kinase (ERK) pathways through ligand‐independent activation of EphA2 (phosphorylation of S897). An <I>in vitro</I> soft agar assay and <I>in vivo</I> orthotopic or subcutaneous tumor model showed that EphA2 enhanced colony formation and accelerated tumor growth, and which seemed to be mainly associated with Akt (T308)/mTORC1 activation. Aberrant expression and activation of EphA2 was also associated with poorer differentiation and higher metastatic ability. Enhanced metastatic ability was also observed in an orthotopic tumor model or lung metastasis model, correlating with Pyk2(Y402)/c‐Src/ERK activation in addition to activation of the canonical Raf/MEK/ERK pathway. The mTORC1 and Raf/Pyk2 pathways also appeared to affect each other. These results suggest that growth factor‐mediated EphA2 might be involved in tumor growth and metastasis through activation of the mTORC1 and Raf/Pyk2 pathways. Therapeutic strategies that target EphA2 and its downstream effectors may be useful to control CC. (H<SMALL>EPATOLOGY</SMALL> 2013;57:2248–2260)</P>
Association between the MDM2 T309G Polymorphism and Leukemia Risk: a Meta-analysis
Yan, Yu-Lan,Han, Feng,Tan, Wen-Min,Wu, Cui-Ping,Qin, Xi Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.16
Several studies have suggested associations between MDM2 (mouse double minute 2 homolog) polymorphisms and leukemia risk, but they reported contradictory results. For better understanding of the effect of MDM2 T309G polymorphism on leukemia risk, we performed a meta-analysis. All eligible studies were identified through a search of PubMed, Web of Science, EMBASE, and Chinese Biomedical Literature (CBM) databases before May 2014. Assessment of associations between the MDM2 T309G polymorphism and leukemia risk was conducted by odds ratios (ORs) and 95% confidence intervals (95% CIs). Finally, a total of 11 publications covering 12 case-control studies with 2, 362 cases and 5, 562 controls concerning MDM2 T309G polymorphism with respect to leukemia were included in the meta-analysis. Significant associations were found between MDM2 T309G polymorphism and leukemia risk in four models in overall populations (G vs T: OR=1.29, 95% CI=1.11-1.49, p=0.001; GG vs TT: OR=1.67, 95% CI=1.21-2.30, p=0.002; GG vs TG/TT: OR=1.56, 95% CI=1.21-2.00, p=0.001; GG/TG vs TT: OR=1.28, 95% CI=1.05-1.57, p=0.015). In the sub-group analysis according to ethnicity, increased leukemia risks were observed in three genetic models among Asians but not Caucasians. In conclusion, the results of our meta-analysis suggest that the MDM2 T309G polymorphism can increase the risk of leukemia, especially among Asian populations.