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<pubDate>Thu, 24 Jul 2008 23:03:59 BST</pubDate>


	<title>CiteULike: Author Park</title>
	<description>CiteULike: Author Park</description>


	<link>http://www.citeulike.org/author/Park</link>
	<dc:publisher>CiteULike.org</dc:publisher>
	<dc:language>en-gb</dc:language>
	<dc:rights>Copyright &#169; 2004-2008 citeulike.org</dc:rights>
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        <rdf:li rdf:resource="http://www.citeulike.org/user/mountain4bike/article/3037899"/>
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<item rdf:about="http://www.citeulike.org/user/paulovn/article/336118">
    <title>Why social networks are different from other types of networks</title>
    <link>http://www.citeulike.org/user/paulovn/article/336118</link>
    <description>&lt;i&gt;(26 May 2003)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;We argue that social networks differ from most other types of networks, including technological and biological networks, in two important ways. First, they have non-trivial clustering or network transitivity, and second, they show positive correlations, also called assortative mixing, between the degrees of adjacent vertices. Social networks are often divided into groups or communities, and it has recently been suggested that this division could account for the observed clustering. We demonstrate that group structure in networks can also account for degree correlations. We show using a simple model that we should expect assortative mixing in such networks whenever there is variation in the sizes of the groups and that the predicted level of assortative mixing compares well with that observed in real-world networks.</description>
    <dc:title>Why social networks are different from other types of networks</dc:title>

    <dc:creator>MEJ Newman</dc:creator>
    <dc:creator>Juyong Park</dc:creator>
    <dc:source>(26 May 2003)</dc:source>
    <dc:date>2005-09-30T09:20:29-00:00</dc:date>
    <prism:publicationYear>2003</prism:publicationYear>
    <prism:category>social-networks</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/joong2/article/3038099">
    <title>Functional rhinoplasty: treatment of the dysfunctional nasal sidewall.</title>
    <link>http://www.citeulike.org/user/joong2/article/3038099</link>
    <description>&lt;i&gt;Facial plastic surgery : FPS, Vol. 22, No. 1. (February 2006), pp. 49-54.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Treatment of nasal obstruction caused by nasal valve dysfunction requires a thorough evaluation of the mechanics of normal nasal anatomy and function. Surgical correction of nasal valve dysfunction is based on determining the epicenter of dysfunction, whether it is a static obstruction of the internal nasal valve or a dynamic collapse of either the external nasal valve or the intervalve area. Spreader grafts, flaring sutures, and butterfly grafts are used to widen and support the narrow internal nasal valve. Alar batten grafts will add support to the collapsing nasal sidewall seen in external nasal valve and intervalve dysfunction. Correction of dynamic collapse from paradoxical concavity of the lateral crura may be obtained from the lateral crural flip-flop graft or by reconstructing the lateral crura using cartilage grafts. A strut graft may correct dynamic obstruction caused by a malformed, easily collapsible lateral crura. This article discusses the evaluation, treatment, and correction of the dysfunctional nasal sidewall and emphasizes the avoidance of iatrogenic damage to the sidewall while performing cosmetic rhinoplasty.</description>
    <dc:title>Functional rhinoplasty: treatment of the dysfunctional nasal sidewall.</dc:title>

    <dc:creator>JA Ballert</dc:creator>
    <dc:creator>SS Park</dc:creator>
    <dc:identifier>doi:10.1055/s-2006-939952</dc:identifier>
    <dc:source>Facial plastic surgery : FPS, Vol. 22, No. 1. (February 2006), pp. 49-54.</dc:source>
    <dc:date>2008-07-24T01:43:39-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Facial plastic surgery : FPS</prism:publicationName>
    <prism:issn>0736-6825</prism:issn>
    <prism:volume>22</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>49</prism:startingPage>
    <prism:endingPage>54</prism:endingPage>
    <prism:category>ogr</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/mountain4bike/article/3037899">
    <title>Single-atom point contact devices fabricated with an atomic force microscope</title>
    <link>http://www.citeulike.org/user/mountain4bike/article/3037899</link>
    <description>&lt;i&gt;Applied Physics Letters, Vol. 69, No. 2. (1996), pp. 269-271.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;View this record in Web of Science</description>
    <dc:title>Single-atom point contact devices fabricated with an atomic force microscope</dc:title>

    <dc:creator>ES Snow</dc:creator>
    <dc:creator>D Park</dc:creator>
    <dc:creator>PM Campbell</dc:creator>
    <dc:source>Applied Physics Letters, Vol. 69, No. 2. (1996), pp. 269-271.</dc:source>
    <dc:date>2008-07-23T22:38:28-00:00</dc:date>
    <prism:publicationYear>1996</prism:publicationYear>
    <prism:publicationName>Applied Physics Letters</prism:publicationName>
    <prism:volume>69</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>269</prism:startingPage>
    <prism:endingPage>271</prism:endingPage>
    <prism:publisher>AIP</prism:publisher>
    <prism:category>pcdiode</prism:category>
    <prism:category>rectenna</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/srp33/article/3037643">
    <title>A Programming Language for Probabilistic Computation</title>
    <link>http://www.citeulike.org/user/srp33/article/3037643</link>
    <description>&lt;i&gt;&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;As probabilistic computations play an increasing role in solving various problems, researchers have designed probabilistic languages to facilitate their modeling. Most of the existing probabilistic languages, however, focus only on discrete distributions, and there has been little effort to develop probabilistic languages whose expressive power is beyond discrete distributions. This dissertation presents a probabilistic language, called PTP (ProbabilisTic Programming), which supports all kinds...</description>
    <dc:title>A Programming Language for Probabilistic Computation</dc:title>

    <dc:creator>Sungwoo Park</dc:creator>
    <dc:date>2008-07-23T19:48:11-00:00</dc:date>
    <prism:category>bayesian_networks</prism:category>
    <prism:category>object_oriented</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/group/1906/article/3037072">
    <title>NahR: effects of replacements at Asn 169 and Arg 248 on promoter binding and inducer recognition</title>
    <link>http://www.citeulike.org/group/1906/article/3037072</link>
    <description>&lt;i&gt;Archives of Biochemistry and Biophysics, Vol. 434, No. 1. (1 February 2005), pp. 67-74.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;NahR, a member of the LysR regulator family, is a positive transcriptional regulator for genes of the naphthalene degradation pathway in Pseudomonas sp. To study NahR binding properties, five single and six double mutants were made at residues 169 and/or 248, which are located in the central inducer recognition domain and the C-terminal multimerization domain of the protein, respectively. The effects of these mutations were examined by monitoring the expression of a firefly luciferase (luc) reporter gene under the control of NahR. We found that all mutants responded to induction by both salicylate and benzoate, whereas the wild-type NahR responded only to salicylate. Mutants N169E, N169E/R248C, and N169E/R248K showed low basal activities with high-level inducer responses, whereas mutant N169D/R248K showed high basal activity with inducer-independent responses. A gel retardation assay demonstrated that the different basal activities might be related to altered binding affinities of the NahR mutants to the Psal promoter. Together, these data suggest that NahR residues 169 and 248 might be involved in DNA binding as well as inducer recognition/binding.</description>
    <dc:title>NahR: effects of replacements at Asn 169 and Arg 248 on promoter binding and inducer recognition</dc:title>

    <dc:creator>Hoo Park</dc:creator>
    <dc:creator>Hae Lee</dc:creator>
    <dc:creator>Woon Lim</dc:creator>
    <dc:creator>Hae Shin</dc:creator>
    <dc:identifier>doi:10.1016/j.abb.2004.10.020</dc:identifier>
    <dc:source>Archives of Biochemistry and Biophysics, Vol. 434, No. 1. (1 February 2005), pp. 67-74.</dc:source>
    <dc:date>2008-07-23T15:15:45-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Archives of Biochemistry and Biophysics</prism:publicationName>
    <prism:volume>434</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>67</prism:startingPage>
    <prism:endingPage>74</prism:endingPage>
    <prism:category>binding</prism:category>
    <prism:category>for-the-review</prism:category>
    <prism:category>inducer</prism:category>
    <prism:category>lysr</prism:category>
    <prism:category>regulation</prism:category>
    <prism:category>transcription</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/mboehmer/article/3036779">
    <title>A Method for Predicting Future Location of Mobile User for Location-based Services System</title>
    <link>http://www.citeulike.org/user/mboehmer/article/3036779</link>
    <description>&lt;i&gt;Computers &#38; Industrial Engineering, Vol. In Press, Accepted Manuscript&lt;/i&gt;</description>
    <dc:title>A Method for Predicting Future Location of Mobile User for Location-based Services System</dc:title>

    <dc:creator>Nhan</dc:creator>
    <dc:creator>Keun Ryu</dc:creator>
    <dc:creator>Nam Park</dc:creator>
    <dc:identifier>doi:10.1016/j.cie.2008.07.009</dc:identifier>
    <dc:source>Computers &#38; Industrial Engineering, Vol. In Press, Accepted Manuscript</dc:source>
    <dc:date>2008-07-23T12:27:04-00:00</dc:date>
    <prism:publicationName>Computers &#38; Industrial Engineering</prism:publicationName>
    <prism:volume>In Press, Accepted Manuscript</prism:volume>
    <prism:category>forecasting</prism:category>
    <prism:category>lbs</prism:category>
    <prism:category>position</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pinyoji/article/3036445">
    <title>Roles of building performance assessment in stakeholder dialogue in AEC</title>
    <link>http://www.citeulike.org/user/pinyoji/article/3036445</link>
    <description>&lt;i&gt;Automation in Construction, Vol. 15, No. 4. (July 2006), pp. 415-427.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;This paper treats rational expressions of building performance in order to better support dialogues between stakeholders in the design process. These expressions are based on the notion of objectively quantifiable performance measures, which are introduced through a set of &#34;performance indicators&#34;. The indicators can be used to quantify expectations and fulfillments in structured dialogues between different stakeholders. Two types of indicators are introduced based on: (1) normative models in biophysics and physiology; and (2) empiricist models of Environment-Behavior studies. The treatment is positioned to support rational decision-making during different stages of building delivery and use. The focus is specifically on the fulfillment of client expectations during design evolution.</description>
    <dc:title>Roles of building performance assessment in stakeholder dialogue in AEC</dc:title>

    <dc:creator>Debajyoti Pati</dc:creator>
    <dc:creator>Cheol-Soo Park</dc:creator>
    <dc:creator>Godfried Augenbroe</dc:creator>
    <dc:identifier>doi:10.1016/j.autcon.2005.06.009</dc:identifier>
    <dc:source>Automation in Construction, Vol. 15, No. 4. (July 2006), pp. 415-427.</dc:source>
    <dc:date>2008-07-23T09:08:25-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Automation in Construction</prism:publicationName>
    <prism:volume>15</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>415</prism:startingPage>
    <prism:endingPage>427</prism:endingPage>
    <prism:category>construction</prism:category>
    <prism:category>performance</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/anar/article/3034779">
    <title>Design and implementation of a wireless sensor network for intelligent light control</title>
    <link>http://www.citeulike.org/user/anar/article/3034779</link>
    <description>&lt;i&gt;(2007), pp. 370-379.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;We present the design and implementation of the Illuminator, a preliminary sensor network-based intelligent light control system for entertainment and media production. Unlike most sensor network applications, which focus on sensing alone, a distinctive aspect of Illuminator is that it closes the loop from light sensing to lighting control. We describe the Illuminator's design requirements, system architecture, algorithms, implementation and experimental results. To satisfy the high-performance light sensing requirements of entertainment and media production applications, the system uses the Illumimote, which is a multi-modal and high fidelity light sensor module well-suited to wireless sensor networks. The Illuminator system is a toolset to characterize the illumination profile of a deployed set of fixed position lights, generate desired lighting effects for moving targets (actors, scenic elements, etc.) based on user constraints expressed in a formal language, and assist in the set up of lights to achieve the same illumination profile in multiple venues. After characterizing deployed lights, the Illuminator computes at run-time optimal light settings to achieve a user-specified actuation profile using an optimization framework based on a genetic algorithm Uniquely, it can use deployed sensors to incorporate changing ambient lighting conditions and moving targets into actuation. With experimental results, we demonstrate that the Illuminator handles various high-level user's constraints and generates optimal light actuation profile. These results suggest that our system should support entertainment and media production applications.</description>
    <dc:title>Design and implementation of a wireless sensor network for intelligent light control</dc:title>

    <dc:creator>Heemin Park</dc:creator>
    <dc:creator>Jeff Burke</dc:creator>
    <dc:creator>Mani Srivastava</dc:creator>
    <dc:identifier>doi:10.1145/1236360.1236407</dc:identifier>
    <dc:source>(2007), pp. 370-379.</dc:source>
    <dc:date>2008-07-22T21:46:58-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:startingPage>370</prism:startingPage>
    <prism:endingPage>379</prism:endingPage>
    <prism:publisher>ACM</prism:publisher>
    <prism:category>entertainment</prism:category>
    <prism:category>intelligent</prism:category>
    <prism:category>iui09_related_work</prism:category>
    <prism:category>light_control</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/satre/article/1969732">
    <title>Finding the evidence for protein-protein interactions from PubMed abstracts.</title>
    <link>http://www.citeulike.org/user/satre/article/1969732</link>
    <description>&lt;i&gt;Bioinformatics, Vol. 22, No. 14. (15 July 2006)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;MOTIVATION: Protein-protein interactions play critical roles in biological processes, and many biologists try to find or to predict crucial information concerning these interactions. Before verifying interactions in biological laboratory work, validating them from previous research is necessary. Although many efforts have been made to create databases that store verified information in a structured form, much interaction information still remains as unstructured text. As the amount of new publications has increased rapidly, a large amount of research has sought to extract interactions from the text automatically. However, there remain various difficulties associated with the process of applying automatically generated results into manually annotated databases. For interactions that are not found in manually stored databases, researchers attempt to search for abstracts or full papers. RESULTS: As a result of a search for two proteins, PubMed frequently returns hundreds of abstracts. In this paper, a method is introduced that validates protein-protein interactions from PubMed abstracts. A query is generated from two given proteins automatically and abstracts are then collected from PubMed. Following this, target proteins and their synonyms are recognized and their interaction information is extracted from the collection. It was found that 67.37% of the interactions from DIP-PPI corpus were found from the PubMed abstracts and 87.37% of interactions were found from the given full texts. AVAILABILITY: Contact authors.</description>
    <dc:title>Finding the evidence for protein-protein interactions from PubMed abstracts.</dc:title>

    <dc:creator>H Jang</dc:creator>
    <dc:creator>J Lim</dc:creator>
    <dc:creator>JH Lim</dc:creator>
    <dc:creator>SJ Park</dc:creator>
    <dc:creator>KC Lee</dc:creator>
    <dc:creator>SH Park</dc:creator>
    <dc:identifier>doi:10.1093/bioinformatics/btl203</dc:identifier>
    <dc:source>Bioinformatics, Vol. 22, No. 14. (15 July 2006)</dc:source>
    <dc:date>2007-11-24T03:16:08-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Bioinformatics</prism:publicationName>
    <prism:issn>1460-2059</prism:issn>
    <prism:volume>22</prism:volume>
    <prism:number>14</prism:number>
    <prism:category>bionlp</prism:category>
    <prism:category>ner</prism:category>
    <prism:category>ppi</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/vmsr/article/3033087">
    <title>Gene expression profile analysis of mouse colon embryonic development.</title>
    <link>http://www.citeulike.org/user/vmsr/article/3033087</link>
    <description>&lt;i&gt;Genesis (New York, N.Y. : 2000), Vol. 41, No. 1. (January 2005), pp. 1-12.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;During late embryogenesis, the mouse colon develops from a pseudostratified, undifferentiated endoderm to a single-layered columnar epithelium with accompanying mesenchymal maturation. To identify regulatory genetic programs underlying these morphological changes, we profiled gene expression of the developing mouse colon by microarray from embryonic day (E)13.5 to E18.5. Unbiased cluster analysis of 13,484 cDNA elements revealed two distinct groups of genes whose expression changes reflect the dynamic morphological events of the epithelium and mesenchyme during this period. Additional analyses revealed two subsets of genes whose expression is either upregulated or downregulated over the same developmental period. Of those genes whose expression increases from E13.5 to E18.5 (n = 158), known functions include acquisition and/or maintenance of colonic differentiation. Genes whose transcription is downregulated over this period (n = 49) have demonstrated roles in nuclear organization, transcriptional regulation, and cell proliferation. These results provide the basis for a molecular portrait of colonic development during late embryogenesis and should be a valuable resource for investigators interested in colonic development and neoplasia, as well as comparative organogenesis.</description>
    <dc:title>Gene expression profile analysis of mouse colon embryonic development.</dc:title>

    <dc:creator>YK Park</dc:creator>
    <dc:creator>JL Franklin</dc:creator>
    <dc:creator>SH Settle</dc:creator>
    <dc:creator>SE Levy</dc:creator>
    <dc:creator>E Chung</dc:creator>
    <dc:creator>LH Jeyakumar</dc:creator>
    <dc:creator>Y Shyr</dc:creator>
    <dc:creator>MK Washington</dc:creator>
    <dc:creator>RH Whitehead</dc:creator>
    <dc:creator>BJ Aronow</dc:creator>
    <dc:creator>RJ Coffey</dc:creator>
    <dc:identifier>doi:10.1002/gene.20088</dc:identifier>
    <dc:source>Genesis (New York, N.Y. : 2000), Vol. 41, No. 1. (January 2005), pp. 1-12.</dc:source>
    <dc:date>2008-07-22T16:09:16-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Genesis (New York, N.Y. : 2000)</prism:publicationName>
    <prism:issn>1526-954X</prism:issn>
    <prism:volume>41</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>1</prism:startingPage>
    <prism:endingPage>12</prism:endingPage>
    <prism:category>vmsr_publications</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/frohike/article/2767211">
    <title>Stromal gene expression predicts clinical outcome in breast cancer</title>
    <link>http://www.citeulike.org/user/frohike/article/2767211</link>
    <description>&lt;i&gt;Nat Med, Vol. 14, No. 5. (May 2008), pp. 518-527.&lt;/i&gt;</description>
    <dc:title>Stromal gene expression predicts clinical outcome in breast cancer</dc:title>

    <dc:creator>Greg Finak</dc:creator>
    <dc:creator>Nicholas Bertos</dc:creator>
    <dc:creator>Francois Pepin</dc:creator>
    <dc:creator>Svetlana Sadekova</dc:creator>
    <dc:creator>Margarita Souleimanova</dc:creator>
    <dc:creator>Hong Zhao</dc:creator>
    <dc:creator>Haiying Chen</dc:creator>
    <dc:creator>Gulbeyaz Omeroglu</dc:creator>
    <dc:creator>Sarkis Meterissian</dc:creator>
    <dc:creator>Atilla Omeroglu</dc:creator>
    <dc:creator>Michael Hallett</dc:creator>
    <dc:creator>Morag Park</dc:creator>
    <dc:identifier>doi:10.1038/nm1764</dc:identifier>
    <dc:source>Nat Med, Vol. 14, No. 5. (May 2008), pp. 518-527.</dc:source>
    <dc:date>2008-05-07T19:39:29-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Nat Med</prism:publicationName>
    <prism:volume>14</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>518</prism:startingPage>
    <prism:endingPage>527</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>breast_cancer</prism:category>
    <prism:category>ismb2008</prism:category>
    <prism:category>microarray</prism:category>
    <prism:category>stroma</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/vmsr/article/3033290">
    <title>Inhibition of epidermal growth factor receptor signaling elevates 15-hydroxyprostaglandin dehydrogenase in non-small-cell lung cancer.</title>
    <link>http://www.citeulike.org/user/vmsr/article/3033290</link>
    <description>&lt;i&gt;Cancer research, Vol. 67, No. 12. (15 June 2007), pp. 5587-5593.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Evidence indicates that the induction of cyclooxygenase-2 (COX-2) and high prostaglandin E2 (PGE2) levels contribute to the pathogenesis of non-small-cell lung cancer (NSCLC). In addition to overproduction by COX-2, PGE2 concentrations also depend upon the levels of the PGE2 catabolic enzyme 15-hydroxyprostaglandin dehydrogenase (15-PGDH). We find a dramatic down-regulation of PGDH protein in NSCLC cell lines and in resected human tumors when compared with matched normal lung. Affymetrix array analysis of 10 normal lung tissue samples and 49 resected lung tumors revealed a much lower expression of PGDH transcripts in all NSCLC histologic groups. In addition, treatment with the epidermal growth factor receptor tyrosine kinase inhibitor (EGFR TKI) erlotinib increased the expression of 15-PGDH in a subset of NSCLC cell lines. This effect may be due in part to an inhibition of the extracellular signal-regulated kinase (ERK) pathway as treatment with mitogen-activated protein kinase kinase (MEK) inhibitor U0126 mimics the erlotinib results. We show by quantitative reverse transcription-PCR that the transcript levels of ZEB1 and Slug transcriptional repressors are dramatically reduced in a responsive cell line upon EGFR and MEK/ERK inhibition. In addition, the Slug protein, but not ZEB1, binds to the PGDH promoter and represses transcription. As these repressors function by recruiting histone deacetylases to promoters, it is likely that PGDH is repressed by an epigenetic mechanism involving histone deacetylation, resulting in increased PGE2 activity in tumors. This effect is reversible in a subset of NSCLC upon treatment with an EGFR TKI.</description>
    <dc:title>Inhibition of epidermal growth factor receptor signaling elevates 15-hydroxyprostaglandin dehydrogenase in non-small-cell lung cancer.</dc:title>

    <dc:creator>L Yang</dc:creator>
    <dc:creator>JM Amann</dc:creator>
    <dc:creator>T Kikuchi</dc:creator>
    <dc:creator>R Porta</dc:creator>
    <dc:creator>M Guix</dc:creator>
    <dc:creator>A Gonzalez</dc:creator>
    <dc:creator>KH Park</dc:creator>
    <dc:creator>D Billheimer</dc:creator>
    <dc:creator>CL Arteaga</dc:creator>
    <dc:creator>HH Tai</dc:creator>
    <dc:creator>R DuBois</dc:creator>
    <dc:creator>DP Carbone</dc:creator>
    <dc:creator>DH Johnson</dc:creator>
    <dc:identifier>doi:10.1158/0008-5472.CAN-06-2287</dc:identifier>
    <dc:source>Cancer research, Vol. 67, No. 12. (15 June 2007), pp. 5587-5593.</dc:source>
    <dc:date>2008-07-22T17:37:20-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Cancer research</prism:publicationName>
    <prism:issn>0008-5472</prism:issn>
    <prism:volume>67</prism:volume>
    <prism:number>12</prism:number>
    <prism:startingPage>5587</prism:startingPage>
    <prism:endingPage>5593</prism:endingPage>
    <prism:category>vmsr_publications</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/vmsr/article/1440939">
    <title>Transcriptional recapitulation and subversion of embryonic colon development by mouse colon tumor models and human colon cancer</title>
    <link>http://www.citeulike.org/user/vmsr/article/1440939</link>
    <description>&lt;i&gt;Genome Biology, Vol. 8 (05 July 2007), R131.&lt;/i&gt;</description>
    <dc:title>Transcriptional recapitulation and subversion of embryonic colon development by mouse colon tumor models and human colon cancer</dc:title>

    <dc:creator>Sergio Kaiser</dc:creator>
    <dc:creator>Young-Kyu Park</dc:creator>
    <dc:creator>Jeffrey Franklin</dc:creator>
    <dc:creator>Richard Halberg</dc:creator>
    <dc:creator>Ming Yu</dc:creator>
    <dc:creator>Walter Jessen</dc:creator>
    <dc:creator>Johannes Freudenberg</dc:creator>
    <dc:creator>Xiaodi Chen</dc:creator>
    <dc:creator>Kevin Haigis</dc:creator>
    <dc:creator>Anil Jegga</dc:creator>
    <dc:creator>Sue Kong</dc:creator>
    <dc:creator>Bhuvaneswari Sakthivel</dc:creator>
    <dc:creator>Huan Xu</dc:creator>
    <dc:creator>Timothy Reichling</dc:creator>
    <dc:creator>Mohammad Azhar</dc:creator>
    <dc:creator>Gregory Boivin</dc:creator>
    <dc:creator>Reade Roberts</dc:creator>
    <dc:creator>Anika Bissahoyo</dc:creator>
    <dc:creator>Fausto Gonzales</dc:creator>
    <dc:creator>Greg Bloom</dc:creator>
    <dc:creator>Stephen Eschrich</dc:creator>
    <dc:creator>Scott Carter</dc:creator>
    <dc:creator>Jeremy Aronow</dc:creator>
    <dc:creator>John Kleimeyer</dc:creator>
    <dc:creator>Michael Kleimeyer</dc:creator>
    <dc:creator>Vivek Ramaswamy</dc:creator>
    <dc:creator>Stephen Settle</dc:creator>
    <dc:creator>Braden Boone</dc:creator>
    <dc:creator>Shawn Levy</dc:creator>
    <dc:creator>Jonathan Graff</dc:creator>
    <dc:creator>Thomas Doetschman</dc:creator>
    <dc:creator>Joanna Groden</dc:creator>
    <dc:creator>William Dove</dc:creator>
    <dc:creator>David Threadgill</dc:creator>
    <dc:creator>Timothy Yeatman</dc:creator>
    <dc:creator>Robert Coffey</dc:creator>
    <dc:creator>Bruce Aronow</dc:creator>
    <dc:identifier>doi:10.1186/gb-2007-8-7-r131</dc:identifier>
    <dc:source>Genome Biology, Vol. 8 (05 July 2007), R131.</dc:source>
    <dc:date>2007-07-07T08:30:31-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Genome Biology</prism:publicationName>
    <prism:issn>1465-6906</prism:issn>
    <prism:volume>8</prism:volume>
    <prism:startingPage>R131</prism:startingPage>
    <prism:category>vmsr_publications</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/ddahlem/article/1611634">
    <title>Discrete-Event Simulation: A First Course</title>
    <link>http://www.citeulike.org/user/ddahlem/article/1611634</link>
    <description>&lt;i&gt;(27 December 2005)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;This volume introduces computational and mathematical techniques for modeling, simulating, and analyzing the performance of various systems. Helps readers gain a better understanding of how systems operate and respond to change by: 1) helping them begin to model, simulate, and analyze simple-but-representative systems as soon as possible; and 2) whenever possible, encouraging the experimental exploration and self-discovery of theoretical results before their formal presentation. Features an approachable writing style that emphasizes concepts and insight without sacrificing rigor. Provides C software as source code for running simulations developed in the book, eliminating the need for readers to do all their programming from scratch. Emphasizes an algorithmic approach throughout. A useful reference for industrial engineers.</description>
    <dc:title>Discrete-Event Simulation: A First Course</dc:title>

    <dc:creator>Lawrence Leemis</dc:creator>
    <dc:creator>Stephen Park</dc:creator>
    <dc:source>(27 December 2005)</dc:source>
    <dc:date>2007-09-01T04:43:02-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publisher>Prentice Hall</prism:publisher>
    <prism:category>2006</prism:category>
    <prism:category>book</prism:category>
    <prism:category>discrete-event</prism:category>
    <prism:category>random-number</prism:category>
    <prism:category>simulation</prism:category>
    <prism:category>statistics</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/viktor21614/article/827819">
    <title>Simple procedures for the construction of a robust and cost-effective cell-free protein synthesis system.</title>
    <link>http://www.citeulike.org/user/viktor21614/article/827819</link>
    <description>&lt;i&gt;J Biotechnol (27 May 2006)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;In this study, as a part of our efforts to improve the robustness and economical feasibility of cell-free protein synthesis, we developed a simple method of preparing the cell extracts used for catalyzing cell-free protein synthesis reactions. We found that the high-speed centrifugation, pre-incubation, and dialysis steps of the conventional procedures could be omitted without losing the translational activity of the resulting cell extract. Instead, a simple centrifugation step at low speed (12,000 RCF for 10min) followed by a brief period of incubation was sufficient for the preparation of an active extract to support cell-free protein synthesis with higher productivity and consistency. Compared to the present standard procedures for the preparation of the S30 extract, the overall cost of the reagents and processing time were reduced by 80 and 60%, respectively.</description>
    <dc:title>Simple procedures for the construction of a robust and cost-effective cell-free protein synthesis system.</dc:title>

    <dc:creator>Tae-Wan Kim</dc:creator>
    <dc:creator>Jung-Won Keum</dc:creator>
    <dc:creator>In-Seok Oh</dc:creator>
    <dc:creator>Cha-Yong Choi</dc:creator>
    <dc:creator>Chang-Gil Park</dc:creator>
    <dc:creator>Dong-Myung Kim</dc:creator>
    <dc:identifier>doi:10.1016/j.jbiotec.2006.05.014</dc:identifier>
    <dc:source>J Biotechnol (27 May 2006)</dc:source>
    <dc:date>2006-09-04T15:17:33-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>J Biotechnol</prism:publicationName>
    <prism:issn>0168-1656</prism:issn>
    <prism:category>cell_free</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/tnhh/article/896748">
    <title>Why social networks are different from other types of networks</title>
    <link>http://www.citeulike.org/user/tnhh/article/896748</link>
    <description>&lt;i&gt;Physical Review E (Statistical, Nonlinear, and Soft Matter Physics), Vol. 68, No. 3. (2003)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;We argue that social networks differ from most other types of networks, including technological and biological networks, in two important ways. First, they have nontrivial clustering or network transitivity and second, they show positive correlations, also called assortative mixing, between the degrees of adjacent vertices. Social networks are often divided into groups or communities, and it has recently been suggested that this division could account for the observed clustering. We demonstrate that group structure in networks can also account for degree correlations. We show using a simple model that we should expect assortative mixing in such networks whenever there is variation in the sizes of the groups and that the predicted level of assortative mixing compares well with that observed in real-world networks.</description>
    <dc:title>Why social networks are different from other types of networks</dc:title>

    <dc:creator>MEJ Newman</dc:creator>
    <dc:creator>Juyong Park</dc:creator>
    <dc:identifier>doi:10.1103/PhysRevE.68.036122</dc:identifier>
    <dc:source>Physical Review E (Statistical, Nonlinear, and Soft Matter Physics), Vol. 68, No. 3. (2003)</dc:source>
    <dc:date>2006-10-14T17:47:33-00:00</dc:date>
    <prism:publicationYear>2003</prism:publicationYear>
    <prism:publicationName>Physical Review E (Statistical, Nonlinear, and Soft Matter Physics)</prism:publicationName>
    <prism:volume>68</prism:volume>
    <prism:number>3</prism:number>
    <prism:publisher>APS</prism:publisher>
    <prism:category>social-networks</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/roboonya/article/3032540">
    <title>Progression of renal allograft histology after renal transplantation in recurrent and nonrecurrent immunoglobulin A nephropathy</title>
    <link>http://www.citeulike.org/user/roboonya/article/3032540</link>
    <description>&lt;i&gt;Human Pathology, Vol. In Press, Corrected Proof&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Summary Little information is available regarding renal histology in cases of chronic allograft dysfunction and graft failure in patients with recurrent immunoglobulin A nephropathy. We compared 57 renal allograft biopsies of 44 patients with recurrent immunoglobulin A nephropathy to 43 biopsies of 33 patients without immunoglobulin A nephropathy recurrence. Clinical parameters such as patient demography and biopsy indications did not differ between the 2 groups, with the exception of time to biopsy. Renal allograft injury, which was assessed by semiquantitative scoring of glomerular, tubulointerstitial, and arteriolar changes, increased linearly over time after transplantation in both recurrent and nonrecurrent samples. Glomerular injuries were significantly correlated with tubulointerstitial injuries in both groups, but the correlation graph reflected an increasing gap in the degrees of tubulointerstitial injury between the 2 groups over time. The levels of glomerulosclerosis, mesangial proliferation, and crescent formation were significantly higher in recurrent samples, whereas the prevalence of chronic rejection was significantly higher in nonrecurrent samples. The presence of segmental sclerosis was associated with significant proteinuria in recurrent samples. Graft survival was better in recurrent immunoglobulin A nephropathy patients than in nonrecurrent patients (74.4% versus 51%) at 10 years after transplantation. In conclusion, slow and progressive glomerular injury is the major cause of long-term graft failure in patients with recurrent immunoglobulin A nephropathy. In contrast, rapidly increasing tubulointerstitial injury is responsible for graft failure in nonrecurrent patients.</description>
    <dc:title>Progression of renal allograft histology after renal transplantation in recurrent and nonrecurrent immunoglobulin A nephropathy</dc:title>

    <dc:creator>Hyeon Jeong</dc:creator>
    <dc:creator>Su-Kil Park</dc:creator>
    <dc:creator>Yong Cho</dc:creator>
    <dc:creator>Myoung Kim</dc:creator>
    <dc:creator>Yu Kim</dc:creator>
    <dc:creator>Jung Choi</dc:creator>
    <dc:creator>Soon Kim</dc:creator>
    <dc:creator>Beom Lim</dc:creator>
    <dc:identifier>doi:10.1016/j.humpath.2008.03.003</dc:identifier>
    <dc:source>Human Pathology, Vol. In Press, Corrected Proof</dc:source>
    <dc:date>2008-07-22T11:09:10-00:00</dc:date>
    <prism:publicationName>Human Pathology</prism:publicationName>
    <prism:volume>In Press, Corrected Proof</prism:volume>
    <prism:category>iga-nephropathy</prism:category>
    <prism:category>transplant</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/satre/article/3031984">
    <title>Identifying the Interaction between Genes and Gene Products Based on Frequently Seen Verbs in Medline Abstracts.</title>
    <link>http://www.citeulike.org/user/satre/article/3031984</link>
    <description>&lt;i&gt;Genome informatics. Workshop on Genome Informatics, Vol. 9 (1998), pp. 62-71.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;We have selected the most frequently seen verbs from raw texts made up of 1-million-words of Medline abstracts, and we were able to identify (or bracket) noun phrases contained in the corpus, with a precision rate of 90%. Then, based on the noun-phrase-bracketted corpus, we tried to find the subject and object terms for some frequently seen verbs in the domain. The precision rate of finding the right subject and object for each verb was about 73%. This task was only made possible because we were able to linguistically analyze (or parse) a large quantity of a raw corpus. Our approach will be useful for classifying genes and gene products and for identifying the interaction between them. It is the first step of our effort in building a genome-related thesaurus and hierarchies in a fully automatic way.</description>
    <dc:title>Identifying the Interaction between Genes and Gene Products Based on Frequently Seen Verbs in Medline Abstracts.</dc:title>

    <dc:creator>T Sekimizu</dc:creator>
    <dc:creator>HS Park</dc:creator>
    <dc:creator>J Tsujii</dc:creator>
    <dc:source>Genome informatics. Workshop on Genome Informatics, Vol. 9 (1998), pp. 62-71.</dc:source>
    <dc:date>2008-07-22T07:24:44-00:00</dc:date>
    <prism:publicationYear>1998</prism:publicationYear>
    <prism:publicationName>Genome informatics. Workshop on Genome Informatics</prism:publicationName>
    <prism:issn>0919-9454</prism:issn>
    <prism:volume>9</prism:volume>
    <prism:startingPage>62</prism:startingPage>
    <prism:endingPage>71</prism:endingPage>
    <prism:category>bionlp</prism:category>
    <prism:category>parsing</prism:category>
    <prism:category>ppi</prism:category>
    <prism:category>rulebased</prism:category>
    <prism:category>textmining</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/balicea/article/3025931">
    <title>Gene by environment interactions.</title>
    <link>http://www.citeulike.org/user/balicea/article/3025931</link>
    <description>&lt;i&gt;Genetic epidemiology, Vol. 31 Suppl 1 (2007)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;This paper summarizes the contributions of group 8 to the Genetic Analysis Workshop 15. Group 8 focused on ways to address the possibility that genetic and environmental effects on phenotype may not be independent, but instead may interact in ways that could play important roles in determining phenotype. Among the eight contributors to this group, all three data sets (expression data, rheumatoid arthritis data, and simulated data) were analyzed. Contributions to this section fell into the two broad categories of refining the data (e.g. stratifying or weighting based on a covariate value) and explicitly modeling the interactions. The contributions also illustrate that there are at least two possible goals for such studies. One goal is simply to identify factors contributing to phenotype in the presence of interactions that might mask the signal to univariate methods. A related but distinct goal is to characterize an interaction (e.g. to determine if the interaction is significant).</description>
    <dc:title>Gene by environment interactions.</dc:title>

    <dc:creator>RC Culverhouse</dc:creator>
    <dc:creator>BK Suarez</dc:creator>
    <dc:creator>L Beckmann</dc:creator>
    <dc:creator>P Chen</dc:creator>
    <dc:creator>YS Chen</dc:creator>
    <dc:creator>YF Chiu</dc:creator>
    <dc:creator>J Chang-Claude</dc:creator>
    <dc:creator>A Dempfle</dc:creator>
    <dc:creator>R Hein</dc:creator>
    <dc:creator>R Kazma</dc:creator>
    <dc:creator>JJ Lebrec</dc:creator>
    <dc:creator>S Lee</dc:creator>
    <dc:creator>S Lim</dc:creator>
    <dc:creator>BS Maher</dc:creator>
    <dc:creator>T Park</dc:creator>
    <dc:creator>H Perdry</dc:creator>
    <dc:creator>KS Wang</dc:creator>
    <dc:creator>PP Wolkow</dc:creator>
    <dc:creator>W Xu</dc:creator>
    <dc:identifier>doi:10.1002/gepi.20282</dc:identifier>
    <dc:source>Genetic epidemiology, Vol. 31 Suppl 1 (2007)</dc:source>
    <dc:date>2008-07-22T00:54:52-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Genetic epidemiology</prism:publicationName>
    <prism:issn>0741-0395</prism:issn>
    <prism:volume>31 Suppl 1</prism:volume>
    <prism:category>bio-stat</prism:category>
    <prism:category>cross-talk</prism:category>
    <prism:category>ecophysiology</prism:category>
    <prism:category>epigenetics</prism:category>
    <prism:category>evolutionary-genomics</prism:category>
    <prism:category>gene-gene</prism:category>
    <prism:category>genome-interactome</prism:category>
    <prism:category>genotype-to-phenotype</prism:category>
    <prism:category>reviews</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/rickl/article/3025878">
    <title>Textual Enhancement of Input: Issues and Possibilities</title>
    <link>http://www.citeulike.org/user/rickl/article/3025878</link>
    <description>&lt;i&gt;Applied Linguistics (6 May 2008), amn010.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The input enhancement hypothesis proposed by Sharwood Smith (1991, 1993) has stimulated considerable research over the last 15 years. This article reviews the research on textual enhancement of input (TE), an area where the majority of input enhancement studies have aggregated. Methodological idiosyncrasies are the norm of this body of research. Seven major issues appear to be limiting the generalizability of the findings and holding up further progress in the understanding of the efficacy of TE for learning: (1) noticing and/or acquisition; (2) TE and comprehension; (3) simultaneous or sequential processing; (4) TE and the nature of the enhanced form; (5) TE and prior knowledge; (6) TE and input flood; and (7) TE and overuse. The existing research has nonetheless offered some important insights that future research should seek to build on. 10.1093/applin/amn010</description>
    <dc:title>Textual Enhancement of Input: Issues and Possibilities</dc:title>

    <dc:creator>Zhaohong Han</dc:creator>
    <dc:creator>Eun Park</dc:creator>
    <dc:creator>Charles Combs</dc:creator>
    <dc:identifier>doi:10.1093/applin/amn010</dc:identifier>
    <dc:source>Applied Linguistics (6 May 2008), amn010.</dc:source>
    <dc:date>2008-07-21T23:53:00-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Applied Linguistics</prism:publicationName>
    <prism:startingPage>amn010</prism:startingPage>
    <prism:category>input</prism:category>
    <prism:category>input_enhancement</prism:category>
    <prism:category>input_flood</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/group/5986/article/3024664">
    <title>The bits and flops of the n-hop multilateration primitive for node localization problems</title>
    <link>http://www.citeulike.org/group/5986/article/3024664</link>
    <description>&lt;i&gt;(2002), pp. 112-121.&lt;/i&gt;</description>
    <dc:title>The bits and flops of the n-hop multilateration primitive for node localization problems</dc:title>

    <dc:creator>Andreas Savvides</dc:creator>
    <dc:creator>Heemin Park</dc:creator>
    <dc:creator>Mani Srivastava</dc:creator>
    <dc:identifier>doi:10.1145/570738.570755</dc:identifier>
    <dc:source>(2002), pp. 112-121.</dc:source>
    <dc:date>2008-07-21T15:09:32-00:00</dc:date>
    <prism:publicationYear>2002</prism:publicationYear>
    <prism:startingPage>112</prism:startingPage>
    <prism:endingPage>121</prism:endingPage>
    <prism:publisher>ACM</prism:publisher>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/satre/article/136657">
    <title>Accomplishments and challenges in literature data mining for biology.</title>
    <link>http://www.citeulike.org/user/satre/article/136657</link>
    <description>&lt;i&gt;Bioinformatics, Vol. 18, No. 12. (December 2002), pp. 1553-1561.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;We review recent results in literature data mining for biology and discuss the need and the steps for a challenge evaluation for this field. Literature data mining has progressed from simple recognition of terms to extraction of interaction relationships from complex sentences, and has broadened from recognition of protein interactions to a range of problems such as improving homology search, identifying cellular location, and so on. To encourage participation and accelerate progress in this expanding field, we propose creating challenge evaluations, and we describe two specific applications in this context.</description>
    <dc:title>Accomplishments and challenges in literature data mining for biology.</dc:title>

    <dc:creator>L Hirschman</dc:creator>
    <dc:creator>JC Park</dc:creator>
    <dc:creator>J Tsujii</dc:creator>
    <dc:creator>L Wong</dc:creator>
    <dc:creator>CH Wu</dc:creator>
    <dc:identifier>doi:10.1093/bioinformatics/18.12.1553</dc:identifier>
    <dc:source>Bioinformatics, Vol. 18, No. 12. (December 2002), pp. 1553-1561.</dc:source>
    <dc:date>2005-03-22T19:00:43-00:00</dc:date>
    <prism:publicationYear>2002</prism:publicationYear>
    <prism:publicationName>Bioinformatics</prism:publicationName>
    <prism:issn>1367-4803</prism:issn>
    <prism:volume>18</prism:volume>
    <prism:number>12</prism:number>
    <prism:startingPage>1553</prism:startingPage>
    <prism:endingPage>1561</prism:endingPage>
    <prism:category>bionlp</prism:category>
    <prism:category>textmining</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/frohike/article/835275">
    <title>The Consensus Coding Sequences of Human Breast and Colorectal Cancers</title>
    <link>http://www.citeulike.org/user/frohike/article/835275</link>
    <description>&lt;i&gt;Science (7 September 2006), 1133427.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The elucidation of the human genome sequence has made it possible to identify genetic alterations in cancers in unprecedented detail. To begin a systematic analysis of such alterations, we have determined the sequence of well-annotated human protein coding genes in two common tumor types. Analysis of 13,023 genes in 11 breast and 11 colorectal cancers revealed that individual tumors accumulate an average of ~90 mutant genes but that only a subset of these contribute to the neoplastic process. Using stringent criteria to delineate this subset, we identified 189 genes (average of 11 per tumor) that were mutated at significant frequency. The vast majority of these genes were not known to be genetically altered in tumors and are predicted to affect a wide range of cellular functions, including transcription, adhesion, and invasion. These data define the genetic landscape of two human cancer types, provide new targets for diagnostic and therapeutic intervention, and open fertile avenues for basic research in tumor biology. 10.1126/science.1133427</description>
    <dc:title>The Consensus Coding Sequences of Human Breast and Colorectal Cancers</dc:title>

    <dc:creator>Tobias Sjoblom</dc:creator>
    <dc:creator>Sian Jones</dc:creator>
    <dc:creator>Laura Wood</dc:creator>
    <dc:creator>Williams Parsons</dc:creator>
    <dc:creator>Jimmy Lin</dc:creator>
    <dc:creator>Thomas Barber</dc:creator>
    <dc:creator>Diana Mandelker</dc:creator>
    <dc:creator>Rebecca Leary</dc:creator>
    <dc:creator>Janine Ptak</dc:creator>
    <dc:creator>Natalie Silliman</dc:creator>
    <dc:creator>Steve Szabo</dc:creator>
    <dc:creator>Phillip Buckhaults</dc:creator>
    <dc:creator>Christopher Farrell</dc:creator>
    <dc:creator>Paul Meeh</dc:creator>
    <dc:creator>Sanford Markowitz</dc:creator>
    <dc:creator>Joseph Willis</dc:creator>
    <dc:creator>Dawn Dawson</dc:creator>
    <dc:creator>James Willson</dc:creator>
    <dc:creator>Adi Gazdar</dc:creator>
    <dc:creator>James Hartigan</dc:creator>
    <dc:creator>Leo Wu</dc:creator>
    <dc:creator>Changsheng Liu</dc:creator>
    <dc:creator>Giovanni Parmigiani</dc:creator>
    <dc:creator>Ben Park</dc:creator>
    <dc:creator>Kurtis Bachman</dc:creator>
    <dc:creator>Nickolas Papadopoulos</dc:creator>
    <dc:creator>Bert Vogelstein</dc:creator>
    <dc:creator>Kenneth Kinzler</dc:creator>
    <dc:creator>Victor Velculescu</dc:creator>
    <dc:identifier>doi:10.1126/science.1133427</dc:identifier>
    <dc:source>Science (7 September 2006), 1133427.</dc:source>
    <dc:date>2006-09-08T10:21:59-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Science</prism:publicationName>
    <prism:startingPage>1133427</prism:startingPage>
    <prism:category>breast_cancer</prism:category>
    <prism:category>coding_sequence</prism:category>
    <prism:category>colorectal_cancer</prism:category>
    <prism:category>ismb2008</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/marck/article/2974233">
    <title>Dichotomies between computational and mathematical models</title>
    <link>http://www.citeulike.org/user/marck/article/2974233</link>
    <description>&lt;i&gt;Nature Biotechnology, Vol. 26, No. 7., pp. 737-738.&lt;/i&gt;</description>
    <dc:title>Dichotomies between computational and mathematical models</dc:title>

    <dc:creator>Anthony Hunt</dc:creator>
    <dc:creator>Glen Ropella</dc:creator>
    <dc:creator>Sunwoo Park</dc:creator>
    <dc:creator>Jesse Engelberg</dc:creator>
    <dc:identifier>doi:10.1038/nbt0708-737</dc:identifier>
    <dc:source>Nature Biotechnology, Vol. 26, No. 7., pp. 737-738.</dc:source>
    <dc:date>2008-07-09T06:30:39-00:00</dc:date>
    <prism:publicationName>Nature Biotechnology</prism:publicationName>
    <prism:issn>1087-0156</prism:issn>
    <prism:volume>26</prism:volume>
    <prism:number>7</prism:number>
    <prism:startingPage>737</prism:startingPage>
    <prism:endingPage>738</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>math</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/group/5599/article/2005737">
    <title>Persistent voids: a new structural metric for membrane fusion</title>
    <link>http://www.citeulike.org/group/5599/article/2005737</link>
    <description>&lt;i&gt;Bioinformatics, Vol. 23, No. 14. (15 July 2007), pp. 1753-1759.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Motivation: Membrane fusion constitutes a key stage in cellular processes such as synaptic neurotransmission and infection by enveloped viruses. Current experimental assays for fusion have thus far been unable to resolve early fusion events in fine structural detail. We have previously used molecular dynamics simulations to develop mechanistic models of fusion by small lipid vesicles. Here, we introduce a novel structural measurement of vesicle topology and fusion geometry: persistent voids. Results: Persistent voids calculations enable systematic measurement of structural changes in vesicle fusion by assessing fusion stalk widths. They also constitute a generally applicable technique for assessing lipid topological change. We use persistent voids to compute dynamic relationships between hemifusion neck widening and formation of a full fusion pore in our simulation data. We predict that a tightly coordinated process of hemifusion neck expansion and pore formation is responsible for the rapid vesicle fusion mechanism, while isolated enlargement of the hemifusion diaphragm leads to the formation of a metastable hemifused intermediate. These findings suggest that rapid fusion between small vesicles proceeds via a small hemifusion diaphragm rather than a fully expanded one. Availability: Software available upon request pending public release. Contact: kasson@cmgm.stanford-edu or pande@stanford.edu Supplementary information: Supplementary data are available on Bioinformatics online. 10.1093/bioinformatics/btm250</description>
    <dc:title>Persistent voids: a new structural metric for membrane fusion</dc:title>

    <dc:creator>Peter Kasson</dc:creator>
    <dc:creator>Afra Zomorodian</dc:creator>
    <dc:creator>Sanghyun Park</dc:creator>
    <dc:creator>Nina Singhal</dc:creator>
    <dc:creator>Leonidas Guibas</dc:creator>
    <dc:creator>Vijay Pande</dc:creator>
    <dc:identifier>doi:10.1093/bioinformatics/btm250</dc:identifier>
    <dc:source>Bioinformatics, Vol. 23, No. 14. (15 July 2007), pp. 1753-1759.</dc:source>
    <dc:date>2007-11-28T15:51:20-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Bioinformatics</prism:publicationName>
    <prism:volume>23</prism:volume>
    <prism:number>14</prism:number>
    <prism:startingPage>1753</prism:startingPage>
    <prism:endingPage>1759</prism:endingPage>
    <prism:category>dartmouth-cs</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/rafagomez/article/3016266">
    <title>Novel inorganic polymer derived microreactors for organic microchemistry applications</title>
    <link>http://www.citeulike.org/user/rafagomez/article/3016266</link>
    <description>&lt;i&gt;Lab Chip (2008)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Microreactors fabricated with optically transparent inorganic polymers from two types of precursors using a UV-microimprinting process demonstrated reliable solvent resistance and capability for performing three model organic synthetic reactions, which were compared with batch systems and glass based microreactors.</description>
    <dc:title>Novel inorganic polymer derived microreactors for organic microchemistry applications</dc:title>

    <dc:creator>Tae-Ho Yoon</dc:creator>
    <dc:creator>Sang-Hee Park</dc:creator>
    <dc:creator>Kyoung-Ik Min</dc:creator>
    <dc:creator>Xunli Zhang</dc:creator>
    <dc:creator>Stephen Haswell</dc:creator>
    <dc:creator>Dong-Pyo Kim</dc:creator>
    <dc:identifier>doi:10.1039/b804726j</dc:identifier>
    <dc:source>Lab Chip (2008)</dc:source>
    <dc:date>2008-07-18T04:40:16-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Lab Chip</prism:publicationName>
    <prism:publisher>The Royal Society of Chemistry</prism:publisher>
    <prism:category>microfluidics</prism:category>
    <prism:category>polymer</prism:category>
    <prism:category>solvent-resistant</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/djmonstermo/article/3015941">
    <title>Antithyroid drug regimen for treating Graves' hyperthyroidism.</title>
    <link>http://www.citeulike.org/user/djmonstermo/article/3015941</link>
    <description>&lt;i&gt;Cochrane database of systematic reviews (Online), No. 2. (2005)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: Antithyroid drugs are widely used in the therapy of hyperthyroidism. There are wide variations in the dose, regimen or duration of treatment used by health professionals. OBJECTIVES: To assess the effects of dose, regimen and duration of antithyroid drug therapy for Graves' hyperthyroidism. SEARCH STRATEGY: We searched the Cochrane Central Register of Controlled Trials (Central), MEDLINE, EMBASE, BIOSIS, CINAHL, HEALTHSTAR, Current Controlled Trials and reference lists. We contacted investigators and hand searched conference abstracts. Most recent search: July 2004. SELECTION CRITERIA: Randomised and quasi-randomised trials of antithyroid medication for Graves' hyperthyroidism were used. DATA COLLECTION AND ANALYSIS: Trial allocation to included, excluded and awaiting assessment categories was made by consensus. Two reviewers independently extracted data and assessed trial quality. Pooling of data for primary outcomes, and select exploratory analyses were undertaken. MAIN RESULTS: Twenty-three randomised trials involving 3115 participants were included. Overall the quality of trials as reported was poor; specifically in terms of allocation concealment, assessor blinding and loss to follow-up. Four trials examined the effect of duration of therapy on relapse rates of Graves' hyperthyroidism. In one trial using the Titration regimen, longer duration therapy (18 months) had significantly fewer relapses (37% versus 58%) than six month therapy (Odds ratio (OR) 0.42, 95% confidence interval (CI) 0.18 to 0.96). In one quasi-randomised trial using the Block-Replace regimen, there was no significant difference between the six and 12 month (relapses rates 41% versus 35%) arms of the study. Extending the duration of therapy to over 18 months was not associated with improved relapse rates (Peto OR 0.75, 95% CI 0.39 to 1.43). Twelve trials examined the effect of Block-Replace versus Titration regimen. The relapse rates were similar in both groups at 51% in the Block-Replace group and 54% in the Titration group (Peto OR 0.86, 95% CI 0.68 to 1.08). Participants reporting rashes (10% versus 5%) and withdrawing due to side effects (16% versus 9%) were significantly higher in the Block-Replace group compared to the Titration group respectively. Three studies considered the addition of thyroxine with continued low dose antithyroid therapy after initial therapy with antithyroid drugs. There was significant heterogeneity between the studies and the difference between the two groups were not significant (Odds ratio 0.58, 95% CI 0.05 to 6.21). Four studies considered the addition of thyroxine alone after initial therapy with antithyroid drugs. There was no significant difference in the relapse rates between the groups after 12 months follow-up with relapse rates being 31% (88/282) with thyroxine and 29% (82/284) with placebo (Peto OR 1.15, 95% CI 0.79 to 1.67). AUTHORS' CONCLUSIONS: The evidence (based on four studies) suggests that the optimal duration of antithyroid drug therapy for the Titration regimen is 12 to 18 months. The six month Block-Replace regimen was found to be as effective as the 12 month treatment in one quasi-randomised study. The Titration (low dose) regimen had fewer adverse effects than the Block-Replace (high dose) regimen and was no less effective in trials (based on 12 trials) of equal duration. Continued thyroxine treatment following initial antithyroid therapy does not appear to provide any benefit in terms of recurrence of hyperthyroidism. The incidence of hypothyroidism was not reported and there were no deaths reported in the study populations.</description>
    <dc:title>Antithyroid drug regimen for treating Graves' hyperthyroidism.</dc:title>

    <dc:creator>P Abraham</dc:creator>
    <dc:creator>A Avenell</dc:creator>
    <dc:creator>WA Watson</dc:creator>
    <dc:creator>CM Park</dc:creator>
    <dc:creator>JS Bevan</dc:creator>
    <dc:identifier>doi:10.1002/14651858.CD003420.pub3</dc:identifier>
    <dc:source>Cochrane database of systematic reviews (Online), No. 2. (2005)</dc:source>
    <dc:date>2008-07-18T00:23:57-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Cochrane database of systematic reviews (Online)</prism:publicationName>
    <prism:issn>1469-493X</prism:issn>
    <prism:number>2</prism:number>
    <prism:category>thyroid</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/hugomallinson/article/3015138">
    <title>Effects of reader interference on the RFID interrogation range</title>
    <link>http://www.citeulike.org/user/hugomallinson/article/3015138</link>
    <description>&lt;i&gt;Microwave Conference, 2007. European (2007), pp. 728-731.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;In this paper, the effects of radio frequency identification (RFID) reader interference are investigated in terms of the interrogation range. In order to evaluate RFID interference quantitatively, the signal-to-interference ratio (SIR) equation is initially derived, and the interrogation-reduction range ratio (IRRR) defined. IRRR is a function of the distance between a desired reader and an interfering reader. Co-channel interference (CCI) and adjacent-channel interference (ACI) instances of IRRR are simulated. Simulation results show that reader-reader distances achieving 0 % IRRR, indicating no interference between the two readers, are 1200 m and 35 m for the CCI and ACI cases, respectively. The IRRR factor is inversely proportional to the reader-reader distance in both cases. The simulation results were also verified by measurement results using an ETRI UHF RFID system. Measurement results were found to be in good agreement with the simulation results. It can be concluded that the present simulation results are reliable and applicable in analyses of more complex interfering problems in actual RFID system deployment instances.</description>
    <dc:title>Effects of reader interference on the RFID interrogation range</dc:title>

    <dc:creator>Do-Yun Kim</dc:creator>
    <dc:creator>Byung-Jun Jang</dc:creator>
    <dc:creator>Hyun-Goo Yoon</dc:creator>
    <dc:creator>Jun-Seok Park</dc:creator>
    <dc:creator>Jong-Gwan Yook</dc:creator>
    <dc:identifier>doi:10.1109/EUMC.2007.4405295</dc:identifier>
    <dc:source>Microwave Conference, 2007. European (2007), pp. 728-731.</dc:source>
    <dc:date>2008-07-17T17:23:39-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Microwave Conference, 2007. European</prism:publicationName>
    <prism:startingPage>728</prism:startingPage>
    <prism:endingPage>731</prism:endingPage>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/hugomallinson/article/3015024">
    <title>Polarization and Space Diversity Antenna Using Inverted-F Antennas for RFID Reader Applications</title>
    <link>http://www.citeulike.org/user/hugomallinson/article/3015024</link>
    <description>&lt;i&gt;Antennas and Wireless Propagation Letters, IEEE, Vol. 5, No. 1. (2006), pp. 265-268.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;An orthogonal antenna is presented for reader applications of radio frequency identification (RFID) at 433 MHz. The antenna is composed of two 1 $times$ 2 subarrays orthogonally placed on a ground plane. Two different feeding networks are introduced to control horizontal and vertical radiation current flows for each subarray, respectively. An inverted-F structure is used as a radiation element with vertical and horizontal currents flowing on the radiator, thereby obtaining two linear polarizations. Antenna gains are 3.71 and 3.43 dBi and isolation between the two input ports is less than 25 dB.</description>
    <dc:title>Polarization and Space Diversity Antenna Using Inverted-F Antennas for RFID Reader Applications</dc:title>

    <dc:creator>JS Kim</dc:creator>
    <dc:creator>KH Shin</dc:creator>
    <dc:creator>SM Park</dc:creator>
    <dc:creator>WK Choi</dc:creator>
    <dc:creator>NS Seong</dc:creator>
    <dc:identifier>doi:10.1109/LAWP.2006.875892</dc:identifier>
    <dc:source>Antennas and Wireless Propagation Letters, IEEE, Vol. 5, No. 1. (2006), pp. 265-268.</dc:source>
    <dc:date>2008-07-17T16:29:36-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Antennas and Wireless Propagation Letters, IEEE</prism:publicationName>
    <prism:volume>5</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>265</prism:startingPage>
    <prism:endingPage>268</prism:endingPage>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/hugomallinson/article/3015019">
    <title>Sensitivity Improvement of the Receiver Module in the Passive Tag Based RFID Reader</title>
    <link>http://www.citeulike.org/user/hugomallinson/article/3015019</link>
    <description>&lt;i&gt;Ubiquitous Intelligence and Computing (2007), pp. 13-22.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;In this paper, we have designed a RFID reader receiver system for improving the performance of the passive Tag based 908.5-914 MHz RFID reader, and analyzed the system performance vis-�-vis frequency, reader, and tag properties. The commercial receiver system causes a loss in sensitivity because of its 24 capacitors and 6 inductors. To improve the overall sensitivity of the receiver, we have designed a system using a circulator, LNA and a SAW filter. The experimental results show that the use of a circulator to separate the Tx/Rx paths eliminates interference, the LNA improves the sensitivity of the Rx module and SAW filter eliminates the noise and spurious components in the received signal.</description>
    <dc:title>Sensitivity Improvement of the Receiver Module in the Passive Tag Based RFID Reader</dc:title>

    <dc:creator>Seunghak Rhee</dc:creator>
    <dc:creator>Jongan Park</dc:creator>
    <dc:creator>Jonghun Chun</dc:creator>
    <dc:identifier>doi:10.1007/978-3-540-73549-6_2</dc:identifier>
    <dc:source>Ubiquitous Intelligence and Computing (2007), pp. 13-22.</dc:source>
    <dc:date>2008-07-17T16:27:49-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Ubiquitous Intelligence and Computing</prism:publicationName>
    <prism:startingPage>13</prism:startingPage>
    <prism:endingPage>22</prism:endingPage>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jyuh/article/3013393">
    <title>E3Miner: a text mining tool for ubiquitin-protein ligases.</title>
    <link>http://www.citeulike.org/user/jyuh/article/3013393</link>
    <description>&lt;i&gt;Nucleic acids research, Vol. 36, No. Web Server issue. (1 July 2008)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Ubiquitination is a regulatory process critically involved in the degradation of &#62;80% of cellular proteins, where such proteins are specifically recognized by a key enzyme, or a ubiquitin-protein ligase (E3). Because of this important role of E3s, a rapidly growing body of the published literature in biology and biomedical fields reports novel findings about various E3s and their molecular mechanisms. However, such findings are neither adequately retrieved by general text-mining tools nor systematically made available by such protein databases as UniProt alone. E3Miner is a web-based text mining tool that extracts and organizes comprehensive knowledge about E3s from the abstracts of journal articles and the relevant databases, supporting users to have a good grasp of E3s and their related information easily from the available text. The tool analyzes text sentences to identify protein names for E3s, to narrow down target substrates and other ubiquitin-transferring proteins in E3-specific ubiquitination pathways and to extract molecular features of E3s during ubiquitination. E3Miner also retrieves E3 data about protein functions, other E3-interacting partners and E3-related human diseases from the protein databases, in order to help facilitate further investigation. E3Miner is freely available through http://e3miner.biopathway.org.</description>
    <dc:title>E3Miner: a text mining tool for ubiquitin-protein ligases.</dc:title>

    <dc:creator>H Lee</dc:creator>
    <dc:creator>GS Yi</dc:creator>
    <dc:creator>JC Park</dc:creator>
    <dc:source>Nucleic acids research, Vol. 36, No. Web Server issue. (1 July 2008)</dc:source>
    <dc:date>2008-07-17T04:31:13-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Nucleic acids research</prism:publicationName>
    <prism:issn>1362-4962</prism:issn>
    <prism:volume>36</prism:volume>
    <prism:number>Web Server issue</prism:number>
    <prism:category>pubmed</prism:category>
    <prism:category>ubiquitin</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/group/1906/article/552040">
    <title>The naphthalene catabolic (nag) genes of Polaromonas naphthalenivorans CJ2: evolutionary implications for two gene clusters and novel regulatory control.</title>
    <link>http://www.citeulike.org/group/1906/article/552040</link>
    <description>&lt;i&gt;Appl Environ Microbiol, Vol. 72, No. 2. (February 2006), pp. 1086-1095.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Polaromonas naphthalenivorans CJ2, found to be responsible for the degradation of naphthalene in situ at a coal tar waste-contaminated site (C.-O. Jeon et al., Proc. Natl. Acad. Sci. USA 100:13591-13596, 2003), is able to grow on mineral salts agar media with naphthalene as the sole carbon source. Beginning from a 484-bp nagAc-like region, we used a genome walking strategy to sequence genes encoding the entire naphthalene degradation pathway andadditional flanking regions. We found that the naphthalene catabolic genes in P. naphthalenivorans CJ2 were divided into one large and one small gene cluster, separated by an unknown distance. The large gene cluster (nagRAaGHAbAcAdBFCQEDJI'ORF1tnpA) is bounded by a LysR-type regulator (nagR). The small cluster (nagR2ORF2I&#34;KL) is bounded by a MarR-type regulator (nagR2). The catabolic genes of P. naphthalenivorans CJ2 were homologous to many of those of Ralstonia U2, which uses the gentisate pathway to convert naphthalene to central metabolites. However, three open reading frames (nagY, nagM, and nagN), present in Ralstonia U2, were absent. Also, P. naphthalenivorans carries two copies of gentisate dioxygenase (nagI) with 77.4% DNA sequence identity to one another and 82% amino acid identity to their homologue in Ralstonia sp. strain U2. Investigation of the operons using reverse transcription PCR showed that each cluster was controlled independently by its respective promoter. Insertional inactivation and lacZ reporter assays showed that nagR2 is a negative regulator and that expression of the small cluster is not induced by naphthalene, salicylate, or gentisate. Association of two putative Azoarcus-related transposases with the large cluster and one Azoarcus-related putative salicylate 5-hydroxylase gene (ORF2) in the small cluster suggests that mobile genetic elements were likely involved in creating the novel arrangement of catabolic and regulatory genes in P. naphthalenivorans.</description>
    <dc:title>The naphthalene catabolic (nag) genes of Polaromonas naphthalenivorans CJ2: evolutionary implications for two gene clusters and novel regulatory control.</dc:title>

    <dc:creator>CO Jeon</dc:creator>
    <dc:creator>M Park</dc:creator>
    <dc:creator>HS Ro</dc:creator>
    <dc:creator>W Park</dc:creator>
    <dc:creator>EL Madsen</dc:creator>
    <dc:identifier>doi:10.1128/AEM.72.2.1086-1095.2006</dc:identifier>
    <dc:source>Appl Environ Microbiol, Vol. 72, No. 2. (February 2006), pp. 1086-1095.</dc:source>
    <dc:date>2006-03-14T20:32:57-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Appl Environ Microbiol</prism:publicationName>
    <prism:issn>0099-2240</prism:issn>
    <prism:volume>72</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>1086</prism:startingPage>
    <prism:endingPage>1095</prism:endingPage>
    <prism:category>biodegradation</prism:category>
    <prism:category>evolution</prism:category>
    <prism:category>for-the-review</prism:category>
    <prism:category>integration</prism:category>
    <prism:category>regulation</prism:category>
    <prism:category>transcription</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/hugomallinson/article/3008590">
    <title>A Passive Circulator with High Isolation using a Directional Coupler for RFID</title>
    <link>http://www.citeulike.org/user/hugomallinson/article/3008590</link>
    <description>&lt;i&gt;Microwave Symposium Digest, 2006. IEEE MTT-S International (2006), pp. 1177-1180.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;In radio-frequency identification (RFID) system, a directional coupler has been used to isolate RX from TX due to its simplicity and low cost compared with a circulator. Nevertheless, a conventional microstrip directional coupler has inherent drawback of poor isolation due to unequal phase velocity between even and odd mode. In this paper, a newly proposed circulator using a microstrip directional coupler is proposed to achieve good isolation between TX and RX. The proposed circulator is used for UHF band RFID reader with a single antenna, of which the operating frequency band is 860 MHz-960 MHz. The measurement of the fabricated circulator using a modified directional coupler exhibits excellent isolation of 64 dB and directivity of 49 dB in its frequency band. The validity of the proposed circulator is demonstrated by comparing the TX leakage at the RX port of RFID reader system with that of a conventional directional coupler</description>
    <dc:title>A Passive Circulator with High Isolation using a Directional Coupler for RFID</dc:title>

    <dc:creator>Wan-Kyu Kim</dc:creator>
    <dc:creator>Moon-Que Lee</dc:creator>
    <dc:creator>Jin-Hyun Kim</dc:creator>
    <dc:creator>Hyung-Sun Lim</dc:creator>
    <dc:creator>Jong-Won Yu</dc:creator>
    <dc:creator>Byung-Jun Jang</dc:creator>
    <dc:creator>Jim-Seok Park</dc:creator>
    <dc:identifier>doi:10.1109/MWSYM.2006.249401</dc:identifier>
    <dc:source>Microwave Symposium Digest, 2006. IEEE MTT-S International (2006), pp. 1177-1180.</dc:source>
    <dc:date>2008-07-16T14:15:45-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Microwave Symposium Digest, 2006. IEEE MTT-S International</prism:publicationName>
    <prism:startingPage>1177</prism:startingPage>
    <prism:endingPage>1180</prism:endingPage>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/gniebler/article/3007909">
    <title>Quasiparticle Energies and Band Gaps in Graphene Nanoribbons</title>
    <link>http://www.citeulike.org/user/gniebler/article/3007909</link>
    <description>&lt;i&gt;Physical Review Letters, Vol. 99, No. 18. (2007)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;We present calculations of the quasiparticle energies and band gaps of graphene nanoribbons (GNRs) carried out using a first-principles many-electron Green's function approach within the GW approximation. Because of the quasi-one-dimensional nature of a GNR, electron-electron interaction effects due to the enhanced screened Coulomb interaction and confinement geometry greatly influence the quasiparticle band gap. Compared with previous tight-binding and density functional theory studies, our calculated quasiparticle band gaps show significant self-energy corrections for both armchair and zigzag GNRs, in the range of 0.5&#8211;3.0&#160;eV for ribbons of width 2.4&#8211;0.4&#160;nm. The quasiparticle band gaps found here suggest that use of GNRs for electronic device components in ambient conditions may be viable.</description>
    <dc:title>Quasiparticle Energies and Band Gaps in Graphene Nanoribbons</dc:title>

    <dc:creator>Li Yang</dc:creator>
    <dc:creator>Cheol Park</dc:creator>
    <dc:creator>Young Son</dc:creator>
    <dc:creator>Marvin Cohen</dc:creator>
    <dc:creator>Steven Louie</dc:creator>
    <dc:identifier>doi:10.1103/PhysRevLett.99.186801</dc:identifier>
    <dc:source>Physical Review Letters, Vol. 99, No. 18. (2007)</dc:source>
    <dc:date>2008-07-16T09:18:12-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Physical Review Letters</prism:publicationName>
    <prism:volume>99</prism:volume>
    <prism:number>18</prism:number>
    <prism:publisher>APS</prism:publisher>
    <prism:category>gnrs</prism:category>
    <prism:category>graphene</prism:category>
    <prism:category>theory</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/qwermish/article/3007880">
    <title>Robust reweighted MAP motion estimation</title>
    <link>http://www.citeulike.org/user/qwermish/article/3007880</link>
    <description>&lt;i&gt;Pattern Analysis and Machine Intelligence, IEEE Transactions on, Vol. 20, No. 4. (1998), pp. 353-365.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;This paper proposes a motion estimation algorithm that is robust to motion discontinuity and noise. The proposed algorithm is constructed by embedding the least median squares (LMedS) of robust statistics into the maximum a posteriori (MAP) estimator. Difficulties in accurate estimation of the motion field arise from the smoothness constraint and the sensitivity to noise. To cope robustly with these problems, a median operator and the concept of reweighted least squares (RLS) are applied to the MAP motion estimator, resulting in the reweighted robust MAP (RRMAP). The proposed RRMAP motion estimation algorithm is also generalized for multiple image frame cases. Computer simulation with various synthetic image sequences shows that the proposed algorithm reduces errors, compared to three existing robust motion estimation algorithms that are based on M-estimation, total least squares (TLS), and Hough transform. It is also observed that the proposed algorithm is statistically efficient and robust to additive Gaussian noise and impulse noise. Furthermore, the proposed algorithm yields reasonable performance for real image sequences</description>
    <dc:title>Robust reweighted MAP motion estimation</dc:title>

    <dc:creator>Dong-Gyu Sim</dc:creator>
    <dc:creator>Rae-Hong Park</dc:creator>
    <dc:identifier>doi:10.1109/34.677261</dc:identifier>
    <dc:source>Pattern Analysis and Machine Intelligence, IEEE Transactions on, Vol. 20, No. 4. (1998), pp. 353-365.</dc:source>
    <dc:date>2008-07-16T08:57:41-00:00</dc:date>
    <prism:publicationYear>1998</prism:publicationYear>
    <prism:publicationName>Pattern Analysis and Machine Intelligence, IEEE Transactions on</prism:publicationName>
    <prism:volume>20</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>353</prism:startingPage>
    <prism:endingPage>365</prism:endingPage>
    <prism:category>imaging</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/eisei/article/3006149">
    <title>Cyclin D2 is an FSH-responsive gene involved in gonadal cell proliferation and oncogenesis.</title>
    <link>http://www.citeulike.org/user/eisei/article/3006149</link>
    <description>&lt;i&gt;Nature, Vol. 384, No. 6608. (5 December 1996), pp. 470-474.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;THE D-type cyclins (D1, D2 and D3) are critical governors of the cell-cycle clock apparatus during the G1 phase of the mammalian cell cycle. These three D-type cyclins are expressed in overlapping, apparently redundant fashion in the proliferating tissues. To investigate why mammalian cells need three distinct D-type cyclins, we have generated mice bearing a disrupted cyclin D2 gene by using gene targeting in embryonic stem cells. Cyclin D2-deficient females are sterile owing to the inability of ovarian granulosa cells to proliferate normally in response to follicle-stimulating hormone (FSH), whereas mutant males display hypoplastic testes. In ovarian granulosa cells, cyclin D2 is specifically induced by FSH via a cyclic-AMP-dependent pathway, indicating that expression of the various D-type cyclins is under control of distinct intracellular signalling pathways. The hypoplasia seen in cyclin D2(-/-) ovaries and testes prompted us to examine human cancers deriving from corresponding tissues. We find that some human ovarian and testicular tumours contain high levels of cyclin D2 messenger RNA.</description>
    <dc:title>Cyclin D2 is an FSH-responsive gene involved in gonadal cell proliferation and oncogenesis.</dc:title>

    <dc:creator>P Sicinski</dc:creator>
    <dc:creator>JL Donaher</dc:creator>
    <dc:creator>Y Geng</dc:creator>
    <dc:creator>SB Parker</dc:creator>
    <dc:creator>H Gardner</dc:creator>
    <dc:creator>MY Park</dc:creator>
    <dc:creator>RL Robker</dc:creator>
    <dc:creator>JS Richards</dc:creator>
    <dc:creator>LK McGinnis</dc:creator>
    <dc:creator>JD Biggers</dc:creator>
    <dc:creator>JJ Eppig</dc:creator>
    <dc:creator>RT Bronson</dc:creator>
    <dc:creator>SJ Elledge</dc:creator>
    <dc:creator>RA Weinberg</dc:creator>
    <dc:identifier>doi:10.1038/384470a0</dc:identifier>
    <dc:source>Nature, Vol. 384, No. 6608. (5 December 1996), pp. 470-474.</dc:source>
    <dc:date>2008-07-15T15:48:39-00:00</dc:date>
    <prism:publicationYear>1996</prism:publicationYear>
    <prism:publicationName>Nature</prism:publicationName>
    <prism:issn>0028-0836</prism:issn>
    <prism:volume>384</prism:volume>
    <prism:number>6608</prism:number>
    <prism:startingPage>470</prism:startingPage>
    <prism:endingPage>474</prism:endingPage>
    <prism:category>cyclin-d1</prism:category>
    <prism:category>cyclins</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/djmonstermo/article/3000873">
    <title>Biliary sludge as a cause of acute pancreatitis.</title>
    <link>http://www.citeulike.org/user/djmonstermo/article/3000873</link>
    <description>&lt;i&gt;The New England journal of medicine, Vol. 326, No. 9. (27 February 1992), pp. 589-593.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND. In about 20 to 40 percent of cases of acute pancreatitis, no cause can be found, and these are labeled idiopathic. In this study, we sought to determine the frequency with which patients with acute idiopathic pancreatitis have biliary sludge, a suspension of cholesterol monohydrate crystals or calcium bilirubinate granules that is found predominantly in the gallbladder. METHODS. Between 1980 and 1988, we prospectively studied 86 patients who had acute pancreatitis. In patients with no known cause of pancreatitis and no ultrasonographic evidence of gallstones or dilatation of the biliary ducts, we determined how often biliary sludge was present and its subsequent fate by repeated microscopical examinations of bile samples and abdominal ultrasonography. The outcome of patients treated by cholecystectomy or papillotomy was compared with that of untreated patients. RESULTS. The pancreatitis was considered idiopathic in 31 of the 86 patients (36 percent), of whom 23 had microscopical evidence of biliary sludge. Biliary sludge was detected by ultrasonography in only 11 of the 23 patients (48 percent). The sludge detected by ultrasonography was composed of calcium bilirubinate granules in 10 and cholesterol monohydrate crystals in 1 (P = 0.003). Calcium bilirubinate granules were found more frequently in men (nine men vs. four women, P less than 0.001). Of the 21 patients in whom biliary sludge was the only finding (2 patients also had dilasted bile ducts when restudied), the 6 treated by cholecystectomy and the 4 treated by papillotomy had fewer recurrences of acute pancreatitis during follow-up (up to seven years) than the 11 untreated patients (P = 0.011). The presence of biliary sludge appeared to increase the likelihood of recurrent attacks of pancreatitis (P = 0.020). CONCLUSIONS. Biliary sludge is an underestimated cause of acute idiopathic pancreatitis.</description>
    <dc:title>Biliary sludge as a cause of acute pancreatitis.</dc:title>

    <dc:creator>SP Lee</dc:creator>
    <dc:creator>JF Nicholls</dc:creator>
    <dc:creator>HZ Park</dc:creator>
    <dc:source>The New England journal of medicine, Vol. 326, No. 9. (27 February 1992), pp. 589-593.</dc:source>
    <dc:date>2008-07-15T03:50:14-00:00</dc:date>
    <prism:publicationYear>1992</prism:publicationYear>
    <prism:publicationName>The New England journal of medicine</prism:publicationName>
    <prism:issn>0028-4793</prism:issn>
    <prism:volume>326</prism:volume>
    <prism:number>9</prism:number>
    <prism:startingPage>589</prism:startingPage>
    <prism:endingPage>593</prism:endingPage>
    <prism:category>gb</prism:category>
    <prism:category>pancreas</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/alexzeh/article/3000110">
    <title>A pipelined VLSI architecture for a list sphere decoder</title>
    <link>http://www.citeulike.org/user/alexzeh/article/3000110</link>
    <description>&lt;i&gt;Circuits and Systems, 2006. ISCAS 2006. Proceedings. 2006 IEEE International Symposium on (2006), 4 pp..&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Since finding the nearest point in a lattice for multi-input multi-output (MIMO) channels is NP-hard, simplified algorithms such as a sphere decoder (SD) have been proposed. With simple modification of SD, a list sphere decoder (LSD), soft information can be extracted for channel decoding and iterative detection/decoding. However, generating such information increases the computational complexity for selecting a specific number of candidate lattice points. In this paper an efficient pipelined VLSI architecture for LSD is presented and its complexity is analyzed. The architecture is constructed with three pipeline stages, two stages for metric calculation units (MCU) and one stage for metric enumeration unit (MEU). It also has three storage units and list units for three successive input MIMO vectors. The pipeline can increase the operating clock frequency and keep one-node-per-cycle policy, so that the average throughput can enhance according to the increment of the clock frequency.</description>
    <dc:title>A pipelined VLSI architecture for a list sphere decoder</dc:title>

    <dc:creator>Jin Lee</dc:creator>
    <dc:creator>Sin-Chong Park</dc:creator>
    <dc:creator>Sungchung Park</dc:creator>
    <dc:identifier>doi:10.1109/ISCAS.2006.1692606</dc:identifier>
    <dc:source>Circuits and Systems, 2006. ISCAS 2006. Proceedings. 2006 IEEE International Symposium on (2006), 4 pp..</dc:source>
    <dc:date>2008-07-14T19:13:18-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Circuits and Systems, 2006. ISCAS 2006. Proceedings. 2006 IEEE International Symposium on</prism:publicationName>
    <prism:startingPage>4 pp.</prism:startingPage>
    <prism:category>coding</prism:category>
    <prism:category>hardware</prism:category>
    <prism:category>list</prism:category>
    <prism:category>vlsi</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/UVA_mag_res/article/2999124">
    <title>Solid-state NMR spectroscopy of a membrane protein in biphenyl phospholipid bicelles with the bilayer normal parallel to the magnetic field</title>
    <link>http://www.citeulike.org/user/UVA_mag_res/article/2999124</link>
    <description>&lt;i&gt;Journal of Magnetic Resonance, Vol. 193, No. 1. (July 2008), pp. 133-138.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Bicelles composed of the long-chain biphenyl phospholipid TBBPC (1-tetradecanoyl-2-(4-(4-biphenyl)butanoyl)-sn-glycero-3-PC) and the short-chain phospholipid DHPC align with their bilayer normals parallel to the direction of the magnetic field. In contrast, in typical bicelles the long-chain phospholipid is DMPC or DPPC, and the bilayers align with their normals perpendicular to the field. Samples of the membrane-bound form of the major coat protein of Pf1 bacteriophage in TBBPC bicelles are stable for several months, align magnetically over a wide range of temperatures, and yield well-resolved solid-state NMR spectra similar to those obtained from samples aligned mechanically on glass plates or in DMPC bicelle samples &#34;flipped&#34; with lanthanide ions so that their bilayer normals are parallel to the field. The order parameter of the TBBPC bicelle sample decreases from approximately 0.9 to 0.8 upon increasing the temperature from 20 °C to 60 °C. Since the frequency spans of the chemical shift and dipolar coupling interactions are twice as large as those obtained from proteins in DMPC bicelles without lanthanide ions, TBBPC bicelles provide an opportunity for structural studies with higher spectral resolution of the metal-binding membrane proteins without the risk of chemical or spectroscopic interference from the added lanthanide ions. In addition, the large temperature range of these samples is advantageous for the studies of membrane proteins that are unstable at elevated temperatures and for experiments requiring measurements as a function of temperature.</description>
    <dc:title>Solid-state NMR spectroscopy of a membrane protein in biphenyl phospholipid bicelles with the bilayer normal parallel to the magnetic field</dc:title>

    <dc:creator>Sang Park</dc:creator>
    <dc:creator>Cécile Loudet</dc:creator>
    <dc:creator>Francesca Marassi</dc:creator>
    <dc:creator>Erick Dufourc</dc:creator>
    <dc:creator>Stanley Opella</dc:creator>
    <dc:identifier>doi:10.1016/j.jmr.2008.04.033</dc:identifier>
    <dc:source>Journal of Magnetic Resonance, Vol. 193, No. 1. (July 2008), pp. 133-138.</dc:source>
    <dc:date>2008-07-14T15:36:58-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Journal of Magnetic Resonance</prism:publicationName>
    <prism:volume>193</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>133</prism:startingPage>
    <prism:endingPage>138</prism:endingPage>
    <prism:category>1</prism:category>
    <prism:category>bilayer</prism:category>
    <prism:category>bill</prism:category>
    <prism:category>membrane</prism:category>
    <prism:category>solid-state</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/reyez/article/2998470">
    <title>Genetic susceptibility to adverse drug reactions</title>
    <link>http://www.citeulike.org/user/reyez/article/2998470</link>
    <description>&lt;i&gt;Trends in Pharmacological Sciences, Vol. 22, No. 6. (1 June 2001), pp. 298-305.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Adverse drug reactions (ADRs) are a major clinical problem. Genetic factors can determine individual susceptibility to both dose-dependent and dose-independent ADRs. Determinants of susceptibility include kinetic factors, such as gene polymorphisms in cytochrome P450 enzymes, and dynamic factors, such as polymorphisms in drug targets. The relative importance of these factors will depend on the nature of the ADR; however, it is likely that more than one gene will be involved in most instances. In the future, whole genome single nucleotide polymorphism (SNP) profiling might allow an unbiased method of determining genetic predisposing factors for ADRs, but might be limited by the lack of adequate numbers of patient samples. The overall clinical utility of genotyping in preventing ADRs needs to be proven by the use of prospective randomized controlled clinical trials.</description>
    <dc:title>Genetic susceptibility to adverse drug reactions</dc:title>

    <dc:creator>Munir Pirmohamed</dc:creator>
    <dc:creator>Kevin Park</dc:creator>
    <dc:identifier>doi:10.1016/S0165-6147(00)01717-X</dc:identifier>
    <dc:source>Trends in Pharmacological Sciences, Vol. 22, No. 6. (1 June 2001), pp. 298-305.</dc:source>
    <dc:date>2008-07-14T09:12:17-00:00</dc:date>
    <prism:publicationYear>2001</prism:publicationYear>
    <prism:publicationName>Trends in Pharmacological Sciences</prism:publicationName>
    <prism:volume>22</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>298</prism:startingPage>
    <prism:endingPage>305</prism:endingPage>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/reyez/article/2998465">
    <title>Cytochrome P450 enzyme polymorphisms and adverse drug reactions</title>
    <link>http://www.citeulike.org/user/reyez/article/2998465</link>
    <description>&lt;i&gt;Toxicology, Vol. 192, No. 1. (1 October 2003), pp. 23-32.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Adverse drug reactions (ADR) are common and many are thought to have a genetic predisposition. There has been a great deal of interest in the role of P450 enzyme gene polymorphisms in the pathogenesis of adverse reactions. The major impact to date of polymorphic P450 expression has been on pre-clinical drug development. However, the direct clinical impact of P450 polymorphisms on prediction of ADRs has been limited, largely because studies have been small and retrospective, and the literature shows an abundance of contradictory data. Furthermore, the clinical- and cost-effectiveness of pre-prescription genotyping for P450 polymorphisms has not been convincingly demonstrated. Further studies that address these deficiencies are urgently needed--only then will prospective P450 genotyping become routine in clinical practice.</description>
    <dc:title>Cytochrome P450 enzyme polymorphisms and adverse drug reactions</dc:title>

    <dc:creator>Munir Pirmohamed</dc:creator>
    <dc:creator>Kevin Park</dc:creator>
    <dc:identifier>doi:10.1016/S0300-483X(03)00247-6</dc:identifier>
    <dc:source>Toxicology, Vol. 192, No. 1. (1 October 2003), pp. 23-32.</dc:source>
    <dc:date>2008-07-14T09:12:09-00:00</dc:date>
    <prism:publicationYear>2003</prism:publicationYear>
    <prism:publicationName>Toxicology</prism:publicationName>
    <prism:volume>192</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>23</prism:startingPage>
    <prism:endingPage>32</prism:endingPage>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/kimschurmann/article/2230216">
    <title>Tactics-based remote execution for mobile computing</title>
    <link>http://www.citeulike.org/user/kimschurmann/article/2230216</link>
    <description>&lt;i&gt;(2003), pp. 273-286.&lt;/i&gt;</description>
    <dc:title>Tactics-based remote execution for mobile computing</dc:title>

    <dc:creator>Rajesh Balan</dc:creator>
    <dc:creator>Mahadev Satyanarayanan</dc:creator>
    <dc:creator>So Park</dc:creator>
    <dc:creator>Tadashi Okoshi</dc:creator>
    <dc:identifier>doi:10.1145/1066116.1066125</dc:identifier>
    <dc:source>(2003), pp. 273-286.</dc:source>
    <dc:date>2008-01-14T12:07:59-00:00</dc:date>
    <prism:publicationYear>2003</prism:publicationYear>
    <prism:startingPage>273</prism:startingPage>
    <prism:endingPage>286</prism:endingPage>
    <prism:publisher>ACM</prism:publisher>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/reyez/article/2908174">
    <title>Crystal structure of the ligand-free G-protein-coupled receptor opsin</title>
    <link>http://www.citeulike.org/user/reyez/article/2908174</link>
    <description>&lt;i&gt;Nature (18 June 2008)&lt;/i&gt;</description>
    <dc:title>Crystal structure of the ligand-free G-protein-coupled receptor opsin</dc:title>

    <dc:creator>Jung Park</dc:creator>
    <dc:creator>Patrick Scheerer</dc:creator>
    <dc:creator>Klaus Hofmann</dc:creator>
    <dc:creator>Hui-Woog Choe</dc:creator>
    <dc:creator>Oliver Ernst</dc:creator>
    <dc:identifier>doi:10.1038/nature07063</dc:identifier>
    <dc:source>Nature (18 June 2008)</dc:source>
    <dc:date>2008-06-19T16:48:32-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Nature</prism:publicationName>
    <prism:issn>0028-0836</prism:issn>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/tsjipko/article/2998343">
    <title>Endothelial cell migration in stable gradients of vascular endothelial growth factor A and fibroblast growth factor 2: effects on chemotaxis and chemokinesis.</title>
    <link>http://www.citeulike.org/user/tsjipko/article/2998343</link>
    <description>&lt;i&gt;The Journal of biological chemistry, Vol. 283, No. 20. (16 May 2008), pp. 13905-13912.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Gradients of secreted signaling proteins guide growing blood vessels during both normal and pathological angiogenesis. However, the mechanisms by which endothelial cells integrate and respond to graded distributions of chemotactic factors are still poorly understood. We have in this study investigated endothelial cell migration in response to hill-shaped gradients of vascular endothelial growth factor A (VEGFA) and fibroblast growth factor 2 (FGF2) using a novel microfluidic chemotaxis chamber (MCC). Cell migration was scored at the level of individual cells using time-lapse microscopy. A stable gradient of VEGFA165 ranging from 0 to 50 ng/ml over a distance of 400 microm was shown to strongly induce chemotaxis of endothelial cells of different vascular origin. VEGFA121, unable to bind proteoglycan and neuropilin coreceptors, was also shown to induce chemotaxis in this setup. Furthermore, a gradient of FGF2 was able to attract venular but not arterial endothelial cells, albeit less efficiently than VEGFA165. Notably, constant levels of VEGFA165, but not of FGF2, were shown to efficiently reduce chemokinesis. Systematic exploration of different gradient shapes led to the identification of a minimal gradient steepness required for efficient cell guidance. Finally, analysis of cell migration in different regions of the applied gradients showed that chemotaxis is reduced when cells reach the high end of the gradient. Our findings suggest that chemotactic growth factor gradients may instruct endothelial cells to shift toward a nonmigratory phenotype when approaching the growth factor source.</description>
    <dc:title>Endothelial cell migration in stable gradients of vascular endothelial growth factor A and fibroblast growth factor 2: effects on chemotaxis and chemokinesis.</dc:title>

    <dc:creator>I Barkefors</dc:creator>
    <dc:creator>S Le Jan</dc:creator>
    <dc:creator>L Jakobsson</dc:creator>
    <dc:creator>E Hejll</dc:creator>
    <dc:creator>G Carlson</dc:creator>
    <dc:creator>H Johansson</dc:creator>
    <dc:creator>J Jarvius</dc:creator>
    <dc:creator>JW Park</dc:creator>
    <dc:creator>N Li Jeon</dc:creator>
    <dc:creator>J Kreuger</dc:creator>
    <dc:identifier>doi:10.1074/jbc.M704917200</dc:identifier>
    <dc:source>The Journal of biological chemistry, Vol. 283, No. 20. (16 May 2008), pp. 13905-13912.</dc:source>
    <dc:date>2008-07-14T07:21:53-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>The Journal of biological chemistry</prism:publicationName>
    <prism:issn>0021-9258</prism:issn>
    <prism:volume>283</prism:volume>
    <prism:number>20</prism:number>
    <prism:startingPage>13905</prism:startingPage>
    <prism:endingPage>13912</prism:endingPage>
    <prism:category>chemotaxis</prism:category>
    <prism:category>fgf</prism:category>
    <prism:category>gradient</prism:category>
    <prism:category>microfluidic</prism:category>
    <prism:category>migration</prism:category>
    <prism:category>vegf</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jyuh/article/908263">
    <title>Characterization of salivary RNA by cDNA library analysis</title>
    <link>http://www.citeulike.org/user/jyuh/article/908263</link>
    <description>&lt;i&gt;Archives of Oral Biology, Vol. In Press, Corrected Proof&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Oral fluid (saliva) meets the demands for a noninvasive and accessible diagnostic medium. Recent reports by our group and others described the presence and use of human RNA in saliva as a diagnostic or forensic tool, including the use for oral cancer detection. To gain insights into the integrity of salivary RNA, we examined in detail the integrity of salivary RNA by generating a cDNA library from pooled supernatant saliva of 10 healthy donors. From a library with a primary library titer of 1.3 x 106 cfu/mL of which 95% of the clones had inserts, we successfully sequenced 117 random colonies containing recombinant clones. BLAST search results indicated that all of these clones contained sequences of human origin. Most of the salivary RNAs appeared to be endonucleolytically cleaved at random positions as indicated by comparisons to respective full length parental RNAs from the Genbank. Twelve of the insert sequences matched to the normal salivary core transcriptome sequences, which are highly abundant mRNAs present in healthy individuals. This study provides an in-depth molecular analysis of the saliva transcriptome and should be a useful resource for future basic and translational studies of RNA in human saliva. In addition, this paper presents unequivocal evidence for the presence of RNA in saliva as determined by the use of diverse techniques such as reverse transcriptase quantitative polymerase chain reaction (RT-qPCR), in vitro translation, and the construction of a salivary cDNA library.</description>
    <dc:title>Characterization of salivary RNA by cDNA library analysis</dc:title>

    <dc:creator>Noh Park</dc:creator>
    <dc:creator>Xiaofeng Zhou</dc:creator>
    <dc:creator>Tianwei Yu</dc:creator>
    <dc:creator>Brigitta Brinkman</dc:creator>
    <dc:creator>Bernhard Zimmermann</dc:creator>
    <dc:creator>Visswanathan Palanisamy</dc:creator>
    <dc:creator>David Wong</dc:creator>
    <dc:identifier>doi:10.1016/j.archoralbio.2006.08.014</dc:identifier>
    <dc:source>Archives of Oral Biology, Vol. In Press, Corrected Proof</dc:source>
    <dc:date>2006-10-20T13:49:50-00:00</dc:date>
    <prism:publicationName>Archives of Oral Biology</prism:publicationName>
    <prism:volume>In Press, Corrected Proof</prism:volume>
    <prism:category>microarray</prism:category>
    <prism:category>saliva</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/booker/article/2997616">
    <title>Sphingosine kinase inhibitor suppresses IL-18-induced interferon-gamma production through inhibition of p38 MAPK activation in human NK cells</title>
    <link>http://www.citeulike.org/user/booker/article/2997616</link>
    <description>&lt;i&gt;Biochemical and Biophysical Research Communications, Vol. In Press, Uncorrected Proof&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Natural killer (NK) cells play an important role in the innate immune response. Interleukin-18 (IL-18) is a well-known interferon-gamma (IFN-[gamma] inducing factor, which stimulates immune response in NK and T cells. Sphingosine kinase (SPHK) catalyzes the formation of sphingosine 1-phosphate (S1P), which acts as a second messenger to function as an anti-apoptotic factor and proliferation stimulator of immune cells. In this study, to elucidate whether SPHK is involved in IL-18-induced IFN-[gamma] production, we measured IL-18-induced IFN-[gamma] production after pre-treatment with SPHK inhibitor (SKI) in NK-92MI cells. We found that IL-18-induced IFN-[gamma] expression was blocked by SKI pre-treatment in both mRNA and protein levels. In addition, the increased IFN-[gamma] production by stimulation with IL-18 is mediated through both SPHK and p38 MAPK. To determine the upstream signals of SKI and p38 MAPK in IL-18-induced IFN-[gamma] production, phosphorylation levels of p38 MAPK was measured after SKI pre-treatment. As a result, inhibition of SPHK by SKI blocked phosphorylation of p38 MAPK, showing that SPHK activation by IL-18 is an upstream signal of p38 MAPK activation. Inhibition of SPHK by SKI also inhibited IL-18-induced IFN-[gamma] production in human primary NK cells. In conclusion, SPHK activation is an essential factor for IL-18-induced IFN-[gamma] production via p38 MAPK.</description>
    <dc:title>Sphingosine kinase inhibitor suppresses IL-18-induced interferon-gamma production through inhibition of p38 MAPK activation in human NK cells</dc:title>

    <dc:creator>Soyoung Cheon</dc:creator>
    <dc:creator>Seok Song</dc:creator>
    <dc:creator>Minkyung Jung</dc:creator>
    <dc:creator>Yoorim Park</dc:creator>
    <dc:creator>Jung-Wook Bang</dc:creator>
    <dc:creator>Tae Kim</dc:creator>
    <dc:creator>Hyunjeong Park</dc:creator>
    <dc:creator>Cherl-Hyun Kim</dc:creator>
    <dc:creator>Yool-Hee Yang</dc:creator>
    <dc:creator>Sa Bang</dc:creator>
    <dc:creator>Daeho Cho</dc:creator>
    <dc:identifier>doi:10.1016/j.bbrc.2008.06.091</dc:identifier>
    <dc:source>Biochemical and Biophysical Research Communications, Vol. In Press, Uncorrected Proof</dc:source>
    <dc:date>2008-07-13T22:41:29-00:00</dc:date>
    <prism:publicationName>Biochemical and Biophysical Research Communications</prism:publicationName>
    <prism:volume>In Press, Uncorrected Proof</prism:volume>
    <prism:category>il-18</prism:category>
    <prism:category>inflammation</prism:category>
    <prism:category>mapk</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/giovanni/article/2996194">
    <title>Mitochondrial iron detoxification is a primary function of frataxin that limits oxidative damage and preserves cell longevity.</title>
    <link>http://www.citeulike.org/user/giovanni/article/2996194</link>
    <description>&lt;i&gt;Human molecular genetics, Vol. 15, No. 3. (1 February 2006), pp. 467-479.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Friedreich ataxia is a severe autosomal-recessive disease characterized by neurodegeneration, cardiomyopathy and diabetes, resulting from reduced synthesis of the mitochondrial protein frataxin. Although frataxin is ubiquitously expressed, frataxin deficiency leads to a selective loss of dorsal root ganglia neurons, cardiomyocytes and pancreatic beta cells. How frataxin normally promotes survival of these particular cells is the subject of intense debate. The predominant view is that frataxin sustains mitochondrial energy production and other cellular functions by providing iron for heme synthesis and iron-sulfur cluster (ISC) assembly and repair. We have proposed that frataxin not only promotes the biogenesis of iron-containing enzymes, but also detoxifies surplus iron thereby affording a critical anti-oxidant mechanism. These two functions have been difficult to tease apart, however, and the physiologic role of iron detoxification by frataxin has not yet been demonstrated in vivo. Here, we describe mutations that specifically impair the ferroxidation or mineralization activity of yeast frataxin, which are necessary for iron detoxification but do not affect the iron chaperone function of the protein. These mutations increase the sensitivity of yeast cells to oxidative stress, shortening chronological life span and precluding survival in the absence of the anti-oxidant enzyme superoxide dismutase. Thus, the role of frataxin is not limited to promoting ISC assembly or heme synthesis. Iron detoxification is another function of frataxin relevant to anti-oxidant defense and cell longevity that could play a critical role in the metabolically demanding environment of non-dividing neuronal, cardiac and pancreatic beta cells.</description>
    <dc:title>Mitochondrial iron detoxification is a primary function of frataxin that limits oxidative damage and preserves cell longevity.</dc:title>

    <dc:creator>O Gakh</dc:creator>
    <dc:creator>S Park</dc:creator>
    <dc:creator>G Liu</dc:creator>
    <dc:creator>L Macomber</dc:creator>
    <dc:creator>JA Imlay</dc:creator>
    <dc:creator>GC Ferreira</dc:creator>
    <dc:creator>G Isaya</dc:creator>
    <dc:source>Human molecular genetics, Vol. 15, No. 3. (1 February 2006), pp. 467-479.</dc:source>
    <dc:date>2008-07-12T15:10:50-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Human molecular genetics</prism:publicationName>
    <prism:issn>0964-6906</prism:issn>
    <prism:volume>15</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>467</prism:startingPage>
    <prism:endingPage>479</prism:endingPage>
    <prism:category>frda</prism:category>
    <prism:category>yeast</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/austin/article/1414733">
    <title>The alliance for cellular signaling plasmid collection: a flexible resource for protein localization studies and signaling pathway analysis.</title>
    <link>http://www.citeulike.org/user/austin/article/1414733</link>
    <description>&lt;i&gt;Mol Cell Proteomics, Vol. 6, No. 3. (March 2007), pp. 413-424.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Cellular responses to inputs that vary both temporally and spatially are determined by complex relationships between the components of cell signaling networks. Analysis of these relationships requires access to a wide range of experimental reagents and techniques, including the ability to express the protein components of the model cells in a variety of contexts. As part of the Alliance for Cellular Signaling, we developed a robust method for cloning large numbers of signaling ORFs into Gateway entry vectors, and we created a wide range of compatible expression platforms for proteomics applications. To date, we have generated over 3000 plasmids that are available to the scientific community via the American Type Culture Collection. We have established a website at www.signaling-gateway.org/data/plasmid/ that allows users to browse, search, and blast Alliance for Cellular Signaling plasmids. The collection primarily contains murine signaling ORFs with an emphasis on kinases and G protein signaling genes. Here we describe the cloning, databasing, and application of this proteomics resource for large scale subcellular localization screens in mammalian cell lines.</description>
    <dc:title>The alliance for cellular signaling plasmid collection: a flexible resource for protein localization studies and signaling pathway analysis.</dc:title>

    <dc:creator>JR Zavzavadjian</dc:creator>
    <dc:creator>S Couture</dc:creator>
    <dc:creator>WS Park</dc:creator>
    <dc:creator>J Whalen</dc:creator>
    <dc:creator>S Lyon</dc:creator>
    <dc:creator>G Lee</dc:creator>
    <dc:creator>E Fung</dc:creator>
    <dc:creator>Q Mi</dc:creator>
    <dc:creator>J Liu</dc:creator>
    <dc:creator>E Wall</dc:creator>
    <dc:creator>L Santat</dc:creator>
    <dc:creator>K Dhandapani</dc:creator>
    <dc:creator>C Kivork</dc:creator>
    <dc:creator>A Driver</dc:creator>
    <dc:creator>X Zhu</dc:creator>
    <dc:creator>MS Chang</dc:creator>
    <dc:creator>B Randhawa</dc:creator>
    <dc:creator>E Gehrig</dc:creator>
    <dc:creator>H Bryan</dc:creator>
    <dc:creator>M Verghese</dc:creator>
    <dc:creator>A Maer</dc:creator>
    <dc:creator>B Saunders</dc:creator>
    <dc:creator>Y Ning</dc:creator>
    <dc:creator>S Subramaniam</dc:creator>
    <dc:creator>T Meyer</dc:creator>
    <dc:creator>MI Simon</dc:creator>
    <dc:creator>N O'Rourke</dc:creator>
    <dc:creator>G Chandy</dc:creator>
    <dc:creator>ID Fraser</dc:creator>
    <dc:identifier>doi:10.1074/mcp.M600437-MCP200</dc:identifier>
    <dc:source>Mol Cell Proteomics, Vol. 6, No. 3. (March 2007), pp. 413-424.</dc:source>
    <dc:date>2007-06-27T02:46:42-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Mol Cell Proteomics</prism:publicationName>
    <prism:issn>1535-9476</prism:issn>
    <prism:volume>6</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>413</prism:startingPage>
    <prism:endingPage>424</prism:endingPage>
    <prism:category>cloning</prism:category>
    <prism:category>gateway</prism:category>
    <prism:category>signaling</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jyuh/article/2987978">
    <title>A Glu487Lys polymorphism in the gene for mitochondrial aldehyde dehydrogenase 2 is associated with myocardial infarction in elderly Korean men</title>
    <link>http://www.citeulike.org/user/jyuh/article/2987978</link>
    <description>&lt;i&gt;Clinica Chimica Acta, Vol. 382, No. 1-2. (July 2007), pp. 43-47.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Background A homozygous mutant (ALDH2*2/*2) of the gene for mitochondrial aldehyde dehydrogenase 2 (ALDH2) at codon 487 was reported to be associated with myocardial infarction (MI) among Japanese men. However, such an association has never been studied in a Korean population.Method The subjects consisted of 122 men (60-81 y) with MI recruited randomly from Yonsei University Medical Center, Korea. A total of 439 men (60-84 y) without MI were selected as controls from the Ansan Geriatric Study. ALDH2 genotypes were determined using the TaqMan fluorogenic 5' nuclease polymerase chain reaction assay.Results Genotypes carrying the mutant ALDH2 allele (ALDH2*1/*2 plus ALDH2*2/*2) were significantly more frequent in patients with MI than in the controls (42.6% vs. 30.5%, P = 0.0163). Multiple logistic regression analysis revealed that ALDH2*1/*2 plus ALDH2*2/*2, together with abnormal high density lipoprotein cholesterol and elevated body mass index, was an independent risk factor for MI in elderly Korean men (odds ratio = 1.976, 95% CI: 1.202-3.248).Conclusions ALDH2 polymorphisms may play an important role in the pathogenesis of MI in elderly Korean men.</description>
    <dc:title>A Glu487Lys polymorphism in the gene for mitochondrial aldehyde dehydrogenase 2 is associated with myocardial infarction in elderly Korean men</dc:title>

    <dc:creator>Sangmee Jo</dc:creator>
    <dc:creator>Eun-Kyung Kim</dc:creator>
    <dc:creator>Moon Park</dc:creator>
    <dc:creator>Changsu Han</dc:creator>
    <dc:creator>Hyun-Young Park</dc:creator>
    <dc:creator>Yangsoo Jang</dc:creator>
    <dc:creator>Byung Song</dc:creator>
    <dc:creator>Inho Jo</dc:creator>
    <dc:identifier>doi:10.1016/j.cca.2007.03.016</dc:identifier>
    <dc:source>Clinica Chimica Acta, Vol. 382, No. 1-2. (July 2007), pp. 43-47.</dc:source>
    <dc:date>2008-07-11T11:02:29-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Clinica Chimica Acta</prism:publicationName>
    <prism:volume>382</prism:volume>
    <prism:number>1-2</prism:number>
    <prism:startingPage>43</prism:startingPage>
    <prism:endingPage>47</prism:endingPage>
    <prism:category>alcohol</prism:category>
    <prism:category>aldh2</prism:category>
    <prism:category>cv</prism:category>
    <prism:category>snp</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/haveuheard/article/2987418">
    <title>An underlying cognitive aspect of design creativity: Limited Commitment Mode control strategy</title>
    <link>http://www.citeulike.org/user/haveuheard/article/2987418</link>
    <description>&lt;i&gt;Design Studies, Vol. 28, No. 6. (November 2007), pp. 585-604.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Design creativity can be enhanced by identifying the underlying cognitive capabilities used by expert designers and training novice designers for those capabilities specifically. It has been identified by Goel that designers use the Limited Commitment Mode (LCM) control strategy in design problem solving. In this work, we conducted a study to confirm that LCM control strategy is used in solving a design problem and to see whether there is a difference in the level of LCM control strategy between expert and student designers. We devised a quantitative measure that can indicate the level of LCM control strategy usage as well as a visual representation for LCM control strategy usage. As a result, through these methods, we concluded that expert designers used more LCM control strategy than student designers. Also, we compared LCM control strategy usage with how soon critical idea decision is made.</description>
    <dc:title>An underlying cognitive aspect of design creativity: Limited Commitment Mode control strategy</dc:title>

    <dc:creator>MH Kim</dc:creator>
    <dc:creator>YS Kim</dc:creator>
    <dc:creator>HS Lee</dc:creator>
    <dc:creator>JA Park</dc:creator>
    <dc:identifier>doi:10.1016/j.destud.2007.04.006</dc:identifier>
    <dc:source>Design Studies, Vol. 28, No. 6. (November 2007), pp. 585-604.</dc:source>
    <dc:date>2008-07-11T09:43:42-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Design Studies</prism:publicationName>
    <prism:volume>28</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>585</prism:startingPage>
    <prism:endingPage>604</prism:endingPage>
    <prism:category>cognitive</prism:category>
    <prism:category>commitment</prism:category>
    <prism:category>creativity</prism:category>
    <prism:category>design</prism:category>
    <prism:category>model</prism:category>
    <prism:category>process</prism:category>
    <prism:category>strategy</prism:category>
</item>



</rdf:RDF>

