205,146 research outputs found
Dr. Lin Sun, CAU, March 2013
No full textThis video is a conversation with Dr. Lin Sun. Dr. Sun talks about an exhibit at the Woodruff Library titled "At The Boundary." Jordan Moore, AUC Woodruff Library, is the interviewer
The stem cell E3-ligase Lin-41 promotes liver cancer progression through inhibition of microRNA-mediated gene silencing
No full textLin-41 is a stem cell-specific E3 ligase and a known target of the tumour suppressor microRNA (miRNA) let-7. Lin-41 was recently reported to mediate ubiquitylation and degradation of the miRNA pathway protein Ago2. We demonstrate that Lin-41 is over-expressed in hepatocellular carcinoma (HCC). Lin-41 over-expression correlates with high a-fetoprotein level, high tumour grade and high tumour stage and predicts early tumour recurrence. Lin-41 is a strong predictor of poor long-term survival for patients with HCC. Lin-41 knock-down by RNA interference in HCC cell lines Huh7 and Hep3B suppressed proliferation in vitro and reduced in vivo tumour growth in NOD/SCID mice. On the other hand, over-expression of Lin-41 in the HCC cell line SK-Hep1 enhanced tumourigenicity. Over-expression and knock-down of Lin-41 led to inverse changes in the levels of Ago1 and Ago2 proteins. Over-expression of Ago1 and Ago2 reduced in vivo tumour growth. Lin-41 over-expression suppressed let-7 activity in HCC cell lines and expression of Lin-41 enhanced the expression of let-7-regulated oncogenes c-Myc, Lin-28B, HMGA2 and type 1 insulin-like growth factor receptor (IGF1R). Expression of Lin-28B and c-Myc enhanced the expression of Lin-41. Chromatin immunoprecipitation and reporter assays revealed direct association of c-Myc with the Lin-41 promoter, resulting in transcriptional transactivation. Our results indicate that Lin-41 plays an important role in the growth of HCC by regulating RISC complex proteins Ago1 and Ago2 to inhibit miRNA-mediated gene silencing and promote the expression of oncogenic proteins. Lin-41 is also a strong prognostic factor for patients with HCC. Copyright (C) 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd
An Analysis of <i>Judge Lin</i>
No full textBiography of Lin Wen Zhong Gong has another way to call, that is Judge Lin. The leading character is Lin Ze-Xu. This book is based on functionary experience of Lin Ze-Xu, with the captivating plots of court case, helping by highly skilled military attach\uc3\ua9s and chivalrous knights, and the history facts of Opium War. It makes Lin Ze-Xu\ue2s Confucian temperament and tragic mood more, also contrasts with author\ue2s sorrow and furiousness for the politics at the time. History, court case, martial arts\ue2\ua6\ue2\ua6etc. are essence of this book and it broadens the way of this writing style.
The topic of the thesis is \ue2An Analysis of Judge Lin\ue2. The following thesis will be divided into six different chapters. The introduction is Chapter one of the thesis, which is including researching motive and purpose, literature review of predecessors, researching version by existing information, raising questions, choosing research methods and arranging chapters. In chapter Two, I discuss the study of characters of Lin Ze-Xu, also makes a deep analysis of author\u27s purpose of writing him. In chapter Three, I analyze supporting actors and actress. Meanwhile, I illustrate author\u27s purpose of writing supporting actress because the author had different manner to describe supporting actress. Moving to the Chapter Four, I mainly focus on the plots of Judge Lin, and organize cases of Lin Ze-Xu and his subordinates to understand features of cases. In Chapter Five, I represent the causes of Opium War. China and England had difference of opinions of opium. Therefore, it is easier to comprehend what the author\u27s purpose is. In the last chapter I summarize the main points of the preceding chapters and confirm particularity of Judge Lin
A fuzzy approach for sequencing interrelated activities in a DSM
No full textProduction and manufacturing systems often involve a myriad of interrelated activities. How these activities are organised and scheduled has a significant effect on the success of a system. Recently, the Design Structure Matrix (DSM) has been regarded as an effective tool for modelling and scheduling interrelated activities. Based on fuzzy set theory, this study explicitly addresses the uncertain activity dependencies in our formulation and develops a mathematical model for sequencing interrelated activities in a DSM. Because of the complexity of the model, a new approach, which embeds an exact algorithm within a framework of a local search heuristic, is presented for solving large problem instances. Testing results demonstrate that relatively good solutions can be easily obtained by our approach, thereby providing managers with an effective tool for scheduling a large number of interrelated activities with uncertain dependencies. © 2012 Copyright Taylor and Francis Group, LLC.Abdelsalam HME, 2006, IEEE T ENG MANAGE, V53, P69, DOI 10.1109-TEM.2005.861805; Ahmadi R, 2001, EUR J OPER RES, V130, P539, DOI 10.1016-S0377-2217(99)00412-9; Banerjee A, 2007, IIE TRANS, V39, P453, DOI 10.1080-07408170601180510; Browning TR, 2001, IEEE T ENG MANAGE, V48, P292, DOI 10.1109-17.946528; Chen CH, 2004, INT J PROD RES, V42, P4623, DOI 10.1080-00207540410001721727; Chen SJ, 2003, COMPUT IND ENG, V44, P435, DOI 10.1016-S0360-8352(02)00230-9; Debels D, 2007, OPER RES, V55, P457, DOI 10.1287-opre.1060.0358; Dubois D., 2000, FUNDAMENTALS FUZZY S; Dubois D, 2003, EUR J OPER RES, V147, P231, DOI 10.1016-S0377-2217(02)00558-1; EPPINGER SD, 1994, RES ENG DES, V6, P1, DOI 10.1007-BF01588087; Eppinger SD, 2001, HARVARD BUS REV, V79, P149; Fortemps P, 1996, FUZZY SET SYST, V82, P319, DOI 10.1016-0165-0114(95)00273-1; Guschinskaya O, 2008, EUR J OPER RES, V189, P902, DOI 10.1016-j.ejor.2006.03.072; Karniel A, 2009, IEEE T ENG MANAGE, V56, P636, DOI 10.1109-TEM.2009.2032032; Karniel A, 2005, COMPUT AIDED DESIGN, V37, P399, DOI 10.1016-j.cad.2004.06.015; KUSIAK A, 1993, INT J PROD RES, V31, P753, DOI 10.1080-00207549308956755; Lancaster J, 2008, INT J PROD RES, V46, P5043, DOI 10.1080-00207540701324176; Li D., 2006, NONLINEAR INTEGER PR; Lin J, 2009, EUR J OPER RES, V196, P1158, DOI 10.1016-j.ejor.2008.05.030; Lin J, 2010, EUR J OPER RES, V201, P737, DOI 10.1016-j.ejor.2009.03.040; Lin J, 2008, EUR J OPER RES, V185, P378, DOI 10.1016-j.ejor.2006.12.022; Luh DB, 2009, CONCURRENT ENG-RES A, V17, P43, DOI 10.1177-1063293X09102249; McCulley C, 1996, STRUCT OPTIMIZATION, V12, P186, DOI 10.1007-BF01196956; Meier C, 2007, J MECH DESIGN, V129, P566, DOI 10.1115-1.2717224; Palpant M, 2004, ANN OPER RES, V131, P237, DOI 10.1023-B:ANOR.0000039521.26237.62; Qian YJ, 2011, IEEE T ENG MANAGE, V58, P688, DOI 10.1109-TEM.2011.2107558; Rowles C. M., 1999, THESIS MIT; Shaja AS, 2010, RES ENG DES, V21, P173, DOI 10.1007-s00163-009-0082-5; Smith RP, 1997, MANAGE SCI, V43, P1104, DOI 10.1287-mnsc.43.8.1104; Smith RP, 1998, CONCURRENT ENG-RES A, V6, P15, DOI 10.1177-1063293X9800600103; Steward D. V., 1981, IEEE T ENG MANAGE, V49, P428; Tang DB, 2010, ADV ENG INFORM, V24, P159, DOI 10.1016-j.aei.2009.08.005; Tang DB, 2000, COMPUT IND ENG, V38, P479, DOI 10.1016-S0360-8352(00)00059-0; Tang DB, 2009, CONCURRENT ENG-RES A, V17, P129, DOI 10.1177-1063293X09105348; YAGER RR, 1981, INFORM SCIENCES, V24, P143, DOI 10.1016-0020-0255(81)90017-7; Yassine A, 2003, CONCURRENT ENG-RES A, V11, P165, DOI 10.1177-106329303034503; Zimmermann H.-J., 1996, FUZZY SET THEORY ITS32
Linoleic acid isomerase activity in enzyme extracts from Lactobacillus acidophilus and Propionibacterium freudenreichii ssp. Shermanii.
No full textA functional variant in the promoter region regulates the C-reactive protein gene and is a potential candidate for increased risk of atrial fibrillation
No full text. Chang S-N, Tsai C-T, Wu C-K, Lee J-K, Lai L-P, Huang S-W, Huang L-Y, Tseng C-D, Lin J-L, Chiang F-T, Hwang J-J (National Taiwan University Hospital Yun-Lin Branch, Yun-Lin; National Taiwan University Hospital, Taipei; National Taiwan University Hospital, Taipei; Institute of Pharmacology, Taipei; and Graduate Institute of Biomedical Engineering, Taipei, Taiwan). A functional variant in the promoter region regulates the C-reactive protein gene and is a potential candidate for increased risk of atrial fibrillation. J Intern Med 2012; 272: 305315. Objectives. In a large population-based cohort, the level of C-reactive protein (CRP) in patients at baseline predicts an increased risk of future development of atrial fibrillation (AF). The mechanism of this increased risk is unknown. Furthermore, both the molecular effects of CRP on atrial myocytes and fibroblasts and whether genetic variants in the CRP gene predispose to AF are also unknown. Methods.similar to A genetic association study between CRP gene polymorphisms and AF was performed in two independent populations (I: 100 AF patients and 101 controls; II: 348 AF patients and 356 controls), with functional studies to elucidate the mechanism of association. Results.similar to Three polymorphisms (T-861C, A-821G and C-390A/C-390T) were found in the 1-kb promoter of CRP. A triallelic polymorphism (C-390A/C-390T) captured all haplotype information and determined the CRP gene promoter activity and the plasma CRP level, and was in nearly complete linkage disequilibrium with G1059C polymorphism in exon 2. The -390A variant was associated with a higher CRP gene promoter activity, a higher plasma CRP level and a higher risk of AF. Patients with AF also had a higher plasma CRP level than controls. CRP significantly increased the inward L-type calcium current in atrial myocytes with no changes in other ionic currents. CRP did not affect the expressions of type I alpha 1 (COL1A1), type III alpha 1 (COL3A1) and type 1 alpha 2 (COL1A2) procollagens in atrial fibroblasts. Conclusion.similar to A CRP gene promoter triallelic polymorphism was associated with CRP gene promoter activity, determined the plasma level of CRP, and predicted the risk of AF. The mechanism of this may be via augmention of calcium influx by CRP in atrial myocytes, but not because of atrial fibrosis
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