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<pubDate>Sun, 27 Jul 2008 07:10:01 BST</pubDate>


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


	<link>http://www.citeulike.org/author/Goto</link>
	<dc:publisher>CiteULike.org</dc:publisher>
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	<dc:rights>Copyright &#169; 2004-2008 citeulike.org</dc:rights>
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        <rdf:li rdf:resource="http://www.citeulike.org/user/dragonrez/article/393111"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/kellyschiabor/article/3034715"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/jerome_ucsf_slb/article/949045"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/kellyschiabor/article/3033133"/>
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<item rdf:about="http://www.citeulike.org/user/MllePapillon/article/3044702">
    <title>Increased generation of reactive oxygen species in embryos cultured in vitro.</title>
    <link>http://www.citeulike.org/user/MllePapillon/article/3044702</link>
    <description>&lt;i&gt;Free radical biology &#38; medicine, Vol. 15, No. 1. (July 1993), pp. 69-75.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Previous studies have suggested that oxygen toxicity is closely related to the developmental blockage of embryos cultured in vitro. In this study, to obtain an actual proof of the increase in production of reactive oxygen species within embryos, we have measured the level of H2O2 in individual embryos using a fluorimetric method. Mouse (ICR) pronuclear stage embryos from the oviducts were cultured for a specified time under various conditions in a medium to which 2',7'-dichlorodihydrofluorescin diacetate was added. After washing the embryos, the fluorescence emissions of the H2O2-dependent oxidative product in embryos were measured. The fluorescent emissions were lowest in embryos cultured under 5% O2 and highest under 40% O2 (5% &#60; 20% &#60; 40%), just the inverse of the culture efficacy. The fluorescence emmissions of embryos cultured in Ham's F-10, which contains hypoxanthine and transition metals such as Cu and Fe, were higher than those cultured in BWW and alpha MEM, which do not contain these components (alpha MEM &#60; BWW &#60; Ham's F-10; again this is the inverse of the culture efficacy). The fluorescence emissions of embryos increased with the time of the exposure to visible light. L-cysteine and thioredoxin, both of which have been shown to promote embryo development, decreased the fluorescence emissions of embryos. All of these results would provide direct evidence for the hypothesis that oxygen radicals are involved in the developmental blockage.</description>
    <dc:title>Increased generation of reactive oxygen species in embryos cultured in vitro.</dc:title>

    <dc:creator>Y Goto</dc:creator>
    <dc:creator>Y Noda</dc:creator>
    <dc:creator>T Mori</dc:creator>
    <dc:creator>M Nakano</dc:creator>
    <dc:source>Free radical biology &#38; medicine, Vol. 15, No. 1. (July 1993), pp. 69-75.</dc:source>
    <dc:date>2008-07-26T12:37:15-00:00</dc:date>
    <prism:publicationYear>1993</prism:publicationYear>
    <prism:publicationName>Free radical biology &#38; medicine</prism:publicationName>
    <prism:issn>0891-5849</prism:issn>
    <prism:volume>15</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>69</prism:startingPage>
    <prism:endingPage>75</prism:endingPage>
    <prism:category>ox_stress_and_ros</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jyuh/article/3043902">
    <title>Primary prevention of cardiovascular disease with pravastatin in Japan (MEGA Study): a prospective randomised controlled trial.</title>
    <link>http://www.citeulike.org/user/jyuh/article/3043902</link>
    <description>&lt;i&gt;Lancet, Vol. 368, No. 9542. (30 September 2006), pp. 1155-1163.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: Evidence-based treatment for hypercholesterolaemia in Japan has been hindered by the lack of direct evidence in this population. Our aim was to assess whether evidence for treatment with statins derived from western populations can be extrapolated to the Japanese population. METHODS: In this prospective, randomised, open-labelled, blinded study, patients with hypercholesterolaemia (total cholesterol 5.69-6.98 mmol/L) and no history of coronary heart disease or stroke were randomly assigned diet or diet plus 10-20 mg pravastatin daily. The primary endpoint was the first occurrence of coronary heart disease. Statistical analyses were done by intention to treat. This trial is registered at ClinicalTrials.gov, number NCT00211705. FINDINGS: 3966 patients were randomly assigned to the diet group and 3866 to the diet plus pravastatin group. Mean follow-up was 5.3 years. At the end of study, 471 and 522 patients had withdrawn, died, or been lost to follow-up in the diet and diet plus pravastatin groups, respectively. Mean total cholesterol was reduced by 2.1% (from 6.27 mmol/L to 6.13 mmol/L) and 11.5% (from 6.27 mmol/L to 5.55 mmol/L) and mean LDL cholesterol by 3.2% (from 4.05 mmol/L to 3.90 mmol/L) and 18.0% (from 4.05 mmol/L to 3.31 mmol/L) in the diet and the diet plus pravastatin groups, respectively. Coronary heart disease was significantly lower in the diet plus pravastatin group than in the diet alone group (66 events vs 101 events; HR 0.67, 95% CI 0.49-0.91; p=0.01). There was no difference in the incidence of malignant neoplasms or other serious adverse events between the two groups. INTERPRETATION: Treatment with a low dose of pravastatin reduces the risk of coronary heart disease in Japan by much the same amount as higher doses have shown in Europe and the USA.</description>
    <dc:title>Primary prevention of cardiovascular disease with pravastatin in Japan (MEGA Study): a prospective randomised controlled trial.</dc:title>

    <dc:creator>H Nakamura</dc:creator>
    <dc:creator>K Arakawa</dc:creator>
    <dc:creator>H Itakura</dc:creator>
    <dc:creator>A Kitabatake</dc:creator>
    <dc:creator>Y Goto</dc:creator>
    <dc:creator>T Toyota</dc:creator>
    <dc:creator>N Nakaya</dc:creator>
    <dc:creator>S Nishimoto</dc:creator>
    <dc:creator>M Muranaka</dc:creator>
    <dc:creator>A Yamamoto</dc:creator>
    <dc:creator>K Mizuno</dc:creator>
    <dc:creator>Y Ohashi</dc:creator>
    <dc:creator></dc:creator>
    <dc:identifier>doi:10.1016/S0140-6736(06)69472-5</dc:identifier>
    <dc:source>Lancet, Vol. 368, No. 9542. (30 September 2006), pp. 1155-1163.</dc:source>
    <dc:date>2008-07-25T23:26:00-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Lancet</prism:publicationName>
    <prism:issn>1474-547X</prism:issn>
    <prism:volume>368</prism:volume>
    <prism:number>9542</prism:number>
    <prism:startingPage>1155</prism:startingPage>
    <prism:endingPage>1163</prism:endingPage>
    <prism:category>cad</prism:category>
    <prism:category>japan</prism:category>
    <prism:category>rct</prism:category>
    <prism:category>statin</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/dragonrez/article/393111">
    <title>The KEGG databases at GenomeNet</title>
    <link>http://www.citeulike.org/user/dragonrez/article/393111</link>
    <description>&lt;i&gt;Nucl. Acids Res., Vol. 30, No. 1. (1 January 2002), pp. 42-46.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The Kyoto Encyclopedia of Genes and Genomes (KEGG) is the primary database resource of the Japanese GenomeNet service (http://www.genome.ad.jp/) for understanding higher order functional meanings and utilities of the cell or the organism from its genome information. KEGG consists of the PATHWAY database for the computerized knowledge on molecular interaction networks such as pathways and complexes, the GENES database for the information about genes and proteins generated by genome sequencing projects, and the LIGAND database for the information about chemical compounds and chemical reactions that are relevant to cellular processes. In addition to these three main databases, limited amounts of experimental data for microarray gene expression profiles and yeast two-hybrid systems are stored in the EXPRESSION and BRITE databases, respectively. Furthermore, a new database, named SSDB, is available for exploring the universe of all protein coding genes in the complete genomes and for identifying functional links and ortholog groups. The data objects in the KEGG databases are all represented as graphs and various computational methods are developed to detect graph features that can be related to biological functions. For example, the correlated clusters are graph similarities which can be used to predict a set of genes coding for a pathway or a complex, as summarized in the ortholog group tables, and the cliques in the SSDB graph are used to annotate genes. The KEGG databases are updated daily and made freely available (http://www.genome.ad.jp/kegg/).</description>
    <dc:title>The KEGG databases at GenomeNet</dc:title>

    <dc:creator>Minoru Kanehisa</dc:creator>
    <dc:creator>Susumu Goto</dc:creator>
    <dc:creator>Shuichi Kawashima</dc:creator>
    <dc:creator>Akihiro Nakaya</dc:creator>
    <dc:source>Nucl. Acids Res., Vol. 30, No. 1. (1 January 2002), pp. 42-46.</dc:source>
    <dc:date>2005-11-15T06:04:39-00:00</dc:date>
    <prism:publicationYear>2002</prism:publicationYear>
    <prism:publicationName>Nucl. Acids Res.</prism:publicationName>
    <prism:volume>30</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>42</prism:startingPage>
    <prism:endingPage>46</prism:endingPage>
    <prism:category>database</prism:category>
    <prism:category>pathway</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/kellyschiabor/article/3034715">
    <title>Association study of the cytochrome P450 17 gene polymorphism with personality traits in healthy subjects.</title>
    <link>http://www.citeulike.org/user/kellyschiabor/article/3034715</link>
    <description>&lt;i&gt;Behavioural brain research (22 June 2008)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;There have been several studies suggesting that sex hormones are involved in characterization of human mental function and behaviour. Recently, it has been reported that the -34T/C polymorphism of cytochrome P450 17 (CYP17) gene affects sex hormone dispositions. Therefore, it is possible that the CYP17 -34T/C polymorphism affects personality traits. In the present study, the association of this genetic polymorphism with personality traits was examined in 595 healthy Japanese. Personality traits were assessed by the Temperament and Character Inventory (TCI), and the CYP17 -34T/C polymorphism was detected by a PCR-RFLP method. In males, the scores of novelty seeking, cooperativeness, and self-transcendence were higher in the group with the C allele than in that without this allele. In females, none of the seven TCI dimensions was different between the two genotype groups. The present study thus suggests that the -34T/C polymorphism of the CYP17 gene affects personality traits of healthy males, but not females, and this gender-dependent effect may be mediated by the action of sex hormones such as estradiol and testosterone.</description>
    <dc:title>Association study of the cytochrome P450 17 gene polymorphism with personality traits in healthy subjects.</dc:title>

    <dc:creator>Yoshihiko Matsumoto</dc:creator>
    <dc:creator>Akihito Suzuki</dc:creator>
    <dc:creator>Naoshi Shibuya</dc:creator>
    <dc:creator>Shingo Oshino</dc:creator>
    <dc:creator>Mitsuhiro Kamata</dc:creator>
    <dc:creator>Kaoru Goto</dc:creator>
    <dc:creator>Koichi Otani</dc:creator>
    <dc:identifier>doi:10.1016/j.bbr.2008.06.017</dc:identifier>
    <dc:source>Behavioural brain research (22 June 2008)</dc:source>
    <dc:date>2008-07-22T20:45:08-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Behavioural brain research</prism:publicationName>
    <prism:issn>0166-4328</prism:issn>
    <prism:category>personality</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jerome_ucsf_slb/article/949045">
    <title>KEGG: kyoto encyclopedia of genes and genomes.</title>
    <link>http://www.citeulike.org/user/jerome_ucsf_slb/article/949045</link>
    <description>&lt;i&gt;Nucleic Acids Res, Vol. 28, No. 1. (1 January 2000), pp. 27-30.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;KEGG (Kyoto Encyclopedia of Genes and Genomes) is a knowledge base for systematic analysis of gene functions, linking genomic information with higher order functional information. The genomic information is stored in the GENES database, which is a collection of gene catalogs for all the completely sequenced genomes and some partial genomes with up-to-date annotation of gene functions. The higher order functional information is stored in the PATHWAY database, which contains graphical representations of cellular processes, such as metabolism, membrane transport, signal transduction and cell cycle. The PATHWAY database is supplemented by a set of ortholog group tables for the information about conserved subpathways (pathway motifs), which are often encoded by positionally coupled genes on the chromosome and which are especially useful in predicting gene functions. A third database in KEGG is LIGAND for the information about chemical compounds, enzyme molecules and enzymatic reactions. KEGG provides Java graphics tools for browsing genome maps, comparing two genome maps and manipulating expression maps, as well as computational tools for sequence comparison, graph comparison and path computation. The KEGG databases are daily updated and made freely available (http://www. genome.ad.jp/kegg/).</description>
    <dc:title>KEGG: kyoto encyclopedia of genes and genomes.</dc:title>

    <dc:creator>M Kanehisa</dc:creator>
    <dc:creator>S Goto</dc:creator>
    <dc:identifier>doi:10.1093/nar/28.1.27</dc:identifier>
    <dc:source>Nucleic Acids Res, Vol. 28, No. 1. (1 January 2000), pp. 27-30.</dc:source>
    <dc:date>2006-11-16T15:20:37-00:00</dc:date>
    <prism:publicationYear>2000</prism:publicationYear>
    <prism:publicationName>Nucleic Acids Res</prism:publicationName>
    <prism:issn>0305-1048</prism:issn>
    <prism:volume>28</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>27</prism:startingPage>
    <prism:endingPage>30</prism:endingPage>
    <prism:category>biogenic_space</prism:category>
    <prism:category>chemical_space</prism:category>
    <prism:category>database</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/kellyschiabor/article/3033133">
    <title>Association study of catechol-O-methyltransferase Val158Met polymorphism with personality traits in Japanese healthy volunteers.</title>
    <link>http://www.citeulike.org/user/kellyschiabor/article/3033133</link>
    <description>&lt;i&gt;European psychiatry : the journal of the Association of European Psychiatrists, Vol. 22, No. 7. (October 2007), pp. 462-465.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Catechol-O-methyltransferase (COMT) is one of the major enzymes for the degradation of catecholamines. It has been suggested that catecholaminergic neurotransmission is involved in characterization of personality. Previous studies on the association between the COMT Val158Met polymorphism and personality traits in healthy subjects have produced inconsistent results. Therefore, the relationship between this polymorphism and personality was re-examined in 478 Japanese healthy volunteers. Personality traits were assessed by the Temperament and Character Inventory (TCI), and the COMT genotypes were determined by a PCR-RFLP method. In total, there were no significant differences among the Val/Val, Val/Met, and Met/Met genotypes in seven TCI dimension scores. Similarly, no significant relationship was found between the COMT genotypes and the TCI dimensions when males and females were analyzed separately. The present study thus suggests that the COMT Val158Met polymorphism is not associated with personality traits in Japanese healthy subjects.</description>
    <dc:title>Association study of catechol-O-methyltransferase Val158Met polymorphism with personality traits in Japanese healthy volunteers.</dc:title>

    <dc:creator>G Ishii</dc:creator>
    <dc:creator>A Suzuki</dc:creator>
    <dc:creator>S Oshino</dc:creator>
    <dc:creator>H Shiraishi</dc:creator>
    <dc:creator>Y Matsumoto</dc:creator>
    <dc:creator>K Otani</dc:creator>
    <dc:creator>K Goto</dc:creator>
    <dc:identifier>doi:10.1016/j.eurpsy.2007.05.005</dc:identifier>
    <dc:source>European psychiatry : the journal of the Association of European Psychiatrists, Vol. 22, No. 7. (October 2007), pp. 462-465.</dc:source>
    <dc:date>2008-07-22T16:21:33-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>European psychiatry : the journal of the Association of European Psychiatrists</prism:publicationName>
    <prism:issn>0924-9338</prism:issn>
    <prism:volume>22</prism:volume>
    <prism:number>7</prism:number>
    <prism:startingPage>462</prism:startingPage>
    <prism:endingPage>465</prism:endingPage>
    <prism:category>comt</prism:category>
    <prism:category>personality</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/mapplab/article/3024821">
    <title>Cooperativity in Transcription Factor Binding to the Coactivator CREB-binding Protein (CBP). THE MIXED LINEAGE LEUKEMIA PROTEIN (MLL) ACTIVATION DOMAIN BINDS TO AN ALLOSTERIC SITE ON THE KIX DOMAIN</title>
    <link>http://www.citeulike.org/user/mapplab/article/3024821</link>
    <description>&lt;i&gt;J. Biol. Chem., Vol. 277, No. 45. (1 November 2002), pp. 43168-43174.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The interactions between cAMP-response element-binding protein (CREB)-binding protein (CBP) and gene-specific transcription factors play an important role in activation of transcription from numerous genes. Cooperative interactions between CBP and multiple transcriptional activators may provide a mechanism for synergistic increases in transcriptional activation. Here we report the characterization of ternary complexes formed by the KIX domain of CBP and the transactivation domain of the trithorax group protein mixed lineage leukemia protein (MLL), together with either the phosphorylated kinase-inducible domain (pKID) of CREB or the activation domain from c-Myb. Isothermal titration calorimetry experiments show that KIX in complex with the MLL activation domain binds the c-Myb activation domain and pKID domain with 2-fold higher affinity than does the KIX domain alone. Thus, the activation domains of Myb and MLL or of pKID and MLL bind cooperatively to KIX. The thermodynamics of these interactions imply different mechanisms of binding cooperativity for the two ternary complexes; the KIXmiddle dotMLLmiddle dotpKID complex is stabilized by entropy increases, whereas the enhancement of Myb binding in the presence of the MLL activation domain is due to more favorable enthalpy. NMR experiments show that the MLL-binding site on KIX is distinct from the surface that binds the pKID and c-Myb activation domains. Our data indicate that KIX can directly mediate cooperative interactions between pairs of transcriptional regulatory proteins. In the case of MLL and c-Myb, both proteins are involved in proliferation of hematopoietic cells and leukemogenesis, and synergistic interactions mediated by CBP may play a functional role. 10.1074/jbc.M207660200</description>
    <dc:title>Cooperativity in Transcription Factor Binding to the Coactivator CREB-binding Protein (CBP). THE MIXED LINEAGE LEUKEMIA PROTEIN (MLL) ACTIVATION DOMAIN BINDS TO AN ALLOSTERIC SITE ON THE KIX DOMAIN</dc:title>

    <dc:creator>Natalie Goto</dc:creator>
    <dc:creator>Tsaffrir Zor</dc:creator>
    <dc:creator>Maria Martinez-Yamout</dc:creator>
    <dc:creator>Jane Dyson</dc:creator>
    <dc:creator>Peter Wright</dc:creator>
    <dc:identifier>doi:10.1074/jbc.M207660200</dc:identifier>
    <dc:source>J. Biol. Chem., Vol. 277, No. 45. (1 November 2002), pp. 43168-43174.</dc:source>
    <dc:date>2008-07-21T16:04:37-00:00</dc:date>
    <prism:publicationYear>2002</prism:publicationYear>
    <prism:publicationName>J. Biol. Chem.</prism:publicationName>
    <prism:volume>277</prism:volume>
    <prism:number>45</prism:number>
    <prism:startingPage>43168</prism:startingPage>
    <prism:endingPage>43174</prism:endingPage>
    <prism:category>cbp</prism:category>
    <prism:category>c-myb</prism:category>
    <prism:category>creb</prism:category>
    <prism:category>kid</prism:category>
    <prism:category>kix</prism:category>
    <prism:category>mll</prism:category>
    <prism:category>nmr</prism:category>
    <prism:category>structure</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/mapplab/article/3024799">
    <title>Structural Basis for Cooperative Transcription Factor Binding to the CBP Coactivator</title>
    <link>http://www.citeulike.org/user/mapplab/article/3024799</link>
    <description>&lt;i&gt;Journal of Molecular Biology, Vol. 355, No. 5. (3 February 2006), pp. 1005-1013.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Regulation of transcription requires interactions between transcriptional activators and transcriptional co-activator CREB binding protein (CBP). The KIX domain of CBP can bind simultaneously to two different proteins, providing an additional mechanism for transcriptional regulation. Here we describe the solution structure of the ternary complex formed by cooperative binding of activation domains from the c-Myb and mixed lineage leukemia (MLL) transcription factors to the KIX domain. The MLL and c-Myb domains form helices that bind to two distinct hydrophobic grooves on opposite faces of KIX. Compared to the binary KIX:c-Myb complex, significant changes are observed in the structure of KIX at the MLL binding interface in the ternary complex. Two regions of KIX that are disordered in the binary complex become structured in the ternary complex: a flexible loop forms intimate contacts with bound MLL, and the C-terminal helix is extended and stabilized by MLL binding. This structural change results in the formation of additional electrostatic/polar interactions between KIX and the bound c-Myb, providing a structural basis for the cooperativity observed for the ternary complex.</description>
    <dc:title>Structural Basis for Cooperative Transcription Factor Binding to the CBP Coactivator</dc:title>

    <dc:creator>Roberto De Guzman</dc:creator>
    <dc:creator>Natalie Goto</dc:creator>
    <dc:creator>Jane Dyson</dc:creator>
    <dc:creator>Peter Wright</dc:creator>
    <dc:identifier>doi:10.1016/j.jmb.2005.09.059</dc:identifier>
    <dc:source>Journal of Molecular Biology, Vol. 355, No. 5. (3 February 2006), pp. 1005-1013.</dc:source>
    <dc:date>2008-07-21T15:59:25-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Journal of Molecular Biology</prism:publicationName>
    <prism:volume>355</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>1005</prism:startingPage>
    <prism:endingPage>1013</prism:endingPage>
    <prism:category>cbp</prism:category>
    <prism:category>c-myb</prism:category>
    <prism:category>kix</prism:category>
    <prism:category>mll</prism:category>
    <prism:category>nmr</prism:category>
    <prism:category>solution</prism:category>
    <prism:category>structure</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/group/1906/article/3024796">
    <title>Emergence of two types of nondechlorinating variants in the tetrachloroethene-halorespiring Desulfitobacterium sp. strain Y51.</title>
    <link>http://www.citeulike.org/group/1906/article/3024796</link>
    <description>&lt;i&gt;Applied microbiology and biotechnology, Vol. 70, No. 6. (May 2006), pp. 720-728.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Desulfitobacterium sp. strain Y51 exhibits a strong dechlorinating activity for tetrachloroethene (PCE), converting it to cis-1,2-dichloroethene via trichloroethene by the action of the PceA reductive dehalogenase (encoded by pceA). The gene organization around the pceA gene cluster was determined to be in the following order: orf4, orf3, ISDesp1, pceA-B-C-T-mcpA, and ISDesp2, where the pceA gene cluster is surrounded by two nearly identical copies of the ISDesp insertion sequence. Serial subculture of strain Y51 gave rise to variants that abolished the PCE-dechlorination activity. Southern hybridization analysis revealed two types of variants termed small deletion (SD) and large deletion (LD). The characterization of both variants revealed a genetic rearrangement around the pceAB gene cluster. In variant SD, ISDesp1 comprised of 1,572 bp was deleted, which includes the tnpAa encoding IS256 family transposase and unknown orf1. The ISDesp1 contained the inverted terminal repeat sequence and a -35 promoter stretch just upstream of the pceA gene, indicating that this IS element is involved in the formation of the variant SD. Loss of the pceA transcription changed the variant SD to the PCE-nondechlorinating phenotype. The variant LD lost the 6.5-kb region, including one copy of ISDesp and the pceABCT-mcpA gene cluster, confirming that the homologous recombination is associated with the emergence of this variant.</description>
    <dc:title>Emergence of two types of nondechlorinating variants in the tetrachloroethene-halorespiring Desulfitobacterium sp. strain Y51.</dc:title>

    <dc:creator>T Futagami</dc:creator>
    <dc:creator>Y Tsuboi</dc:creator>
    <dc:creator>A Suyama</dc:creator>
    <dc:creator>M Goto</dc:creator>
    <dc:creator>K Furukawa</dc:creator>
    <dc:identifier>doi:10.1007/s00253-005-0112-9</dc:identifier>
    <dc:source>Applied microbiology and biotechnology, Vol. 70, No. 6. (May 2006), pp. 720-728.</dc:source>
    <dc:date>2008-07-21T15:57:28-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Applied microbiology and biotechnology</prism:publicationName>
    <prism:issn>0175-7598</prism:issn>
    <prism:volume>70</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>720</prism:startingPage>
    <prism:endingPage>728</prism:endingPage>
    <prism:category>biodegradation</prism:category>
    <prism:category>for-the-review</prism:category>
    <prism:category>new-enzyme</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/cactus/article/3017516">
    <title>Structural stability of amyloid fibrils of [beta]2-microglobulin in comparison with its native fold</title>
    <link>http://www.citeulike.org/user/cactus/article/3017516</link>
    <description>&lt;i&gt;Biochimica et Biophysica Acta (BBA) - Proteins &#38; Proteomics, Vol. 1753, No. 1. (10 November 2005), pp. 64-75.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Among various amyloidogenic proteins, [beta]2-microglobulin ([beta]2-m) responsible for dialysis-related amyloidosis is a target of extensive study because of its clinical importance and suitable size for examining the formation of amyloid fibrils in comparison with protein folding to the native state. The structure and stability of amyloid fibrils have been studied with various physicochemical methods, including H/D exchange of amyloid fibrils combined with dissolution of fibrils by dimethylsulfoxide and NMR analysis, thermodynamic analysis of amyloid fibril formation by isothermal calorimetry, and analysis of the effects of pressure on the structure of amyloid fibrils. The results are consistent with the view that amyloid fibrils are a main-chain-dominated structure with larger numbers of hydrogen bonds and pressure-accessible cavities in the interior, in contrast to the side-chain-dominated native structure with the optimal packing of amino acid residues. We consider that a main-chain dominated structure provides the structural basis for various conformational states even with one protein. When this feature is combined with another unique feature, template-dependent growth, propagation and maturation of the amyloid conformation, which cannot be predicted with Anfinsen's dogma, take place.</description>
    <dc:title>Structural stability of amyloid fibrils of [beta]2-microglobulin in comparison with its native fold</dc:title>

    <dc:creator>Eri Chatani</dc:creator>
    <dc:creator>Yuji Goto</dc:creator>
    <dc:identifier>doi:10.1016/j.bbapap.2005.08.002</dc:identifier>
    <dc:source>Biochimica et Biophysica Acta (BBA) - Proteins &#38; Proteomics, Vol. 1753, No. 1. (10 November 2005), pp. 64-75.</dc:source>
    <dc:date>2008-07-18T10:42:57-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Biochimica et Biophysica Acta (BBA) - Proteins &#38; Proteomics</prism:publicationName>
    <prism:volume>1753</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>64</prism:startingPage>
    <prism:endingPage>75</prism:endingPage>
    <prism:category>amyloid</prism:category>
    <prism:category>experiment</prism:category>
    <prism:category>microglobulin</prism:category>
    <prism:category>stability</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jyuh/article/2819747">
    <title>KEGG Atlas mapping for global analysis of metabolic pathways</title>
    <link>http://www.citeulike.org/user/jyuh/article/2819747</link>
    <description>&lt;i&gt;Nucl. Acids Res. (13 May 2008), gkn282.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;KEGG Atlas is a new graphical interface to the KEGG suite of databases, especially to the systems information in the PATHWAY and BRITE databases. It currently consists of a single global map and an associated viewer for metabolism, covering about 120 KEGG metabolic pathway maps and about 10 BRITE hierarchies. The viewer allows the user to navigate and zoom the global map under the Ajax technology. The mapping of high-throughput experimental data onto the global map is the main use of KEGG Atlas. In the global metabolism map, the node (circle) is a chemical compound and the edge (line) is a set of reactions linked to a set of KEGG Orthology (KO) entries for enzyme genes. Once gene identifiers in different organisms are converted to the K number identifiers in the KO system, corresponding line segments can be highlighted in the global map, allowing the user to view genome sequence data as organism-specific pathways, gene expression data as up- or down-regulated pathways, etc. Once chemical compounds are converted to the C number identifiers in KEGG, metabolomics data can also be displayed in the global map. KEGG Atlas is available at http://www.genome.jp/kegg/atlas/. 10.1093/nar/gkn282</description>
    <dc:title>KEGG Atlas mapping for global analysis of metabolic pathways</dc:title>

    <dc:creator>Shujiro Okuda</dc:creator>
    <dc:creator>Takuji Yamada</dc:creator>
    <dc:creator>Masami Hamajima</dc:creator>
    <dc:creator>Masumi Itoh</dc:creator>
    <dc:creator>Toshiaki Katayama</dc:creator>
    <dc:creator>Peer Bork</dc:creator>
    <dc:creator>Susumu Goto</dc:creator>
    <dc:creator>Minoru Kanehisa</dc:creator>
    <dc:identifier>doi:10.1093/nar/gkn282</dc:identifier>
    <dc:source>Nucl. Acids Res. (13 May 2008), gkn282.</dc:source>
    <dc:date>2008-05-21T12:32:21-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Nucl. Acids Res.</prism:publicationName>
    <prism:startingPage>gkn282</prism:startingPage>
    <prism:category>pathway</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/group/1906/article/523276">
    <title>Biphenyl dioxygenases: functional versatilities and directed evolution.</title>
    <link>http://www.citeulike.org/group/1906/article/523276</link>
    <description>&lt;i&gt;J Bacteriol, Vol. 186, No. 16. (August 2004), pp. 5189-5196.&lt;/i&gt;</description>
    <dc:title>Biphenyl dioxygenases: functional versatilities and directed evolution.</dc:title>

    <dc:creator>K Furukawa</dc:creator>
    <dc:creator>H Suenaga</dc:creator>
    <dc:creator>M Goto</dc:creator>
    <dc:identifier>doi:10.1128/JB.186.16.5189-5196.2004</dc:identifier>
    <dc:source>J Bacteriol, Vol. 186, No. 16. (August 2004), pp. 5189-5196.</dc:source>
    <dc:date>2006-02-27T10:14:56-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>J Bacteriol</prism:publicationName>
    <prism:issn>0021-9193</prism:issn>
    <prism:volume>186</prism:volume>
    <prism:number>16</prism:number>
    <prism:startingPage>5189</prism:startingPage>
    <prism:endingPage>5196</prism:endingPage>
    <prism:category>biodegradation</prism:category>
    <prism:category>evolution</prism:category>
    <prism:category>for-the-review</prism:category>
    <prism:category>regulation</prism:category>
    <prism:category>transcription</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/group/1906/article/3008988">
    <title>Cross-Regulation of Biphenyl- and Salicylate-Catabolic Genes by Two Regulatory Systems in Pseudomonas pseudoalcaligenes KF707</title>
    <link>http://www.citeulike.org/group/1906/article/3008988</link>
    <description>&lt;i&gt;J. Bacteriol., Vol. 188, No. 13. (1 July 2006), pp. 4690-4697.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Pseudomonas pseudoalcaligenes KF707 grows on biphenyl and salicylate as sole sources of carbon. The biphenyl-catabolic (bph) genes are organized as bphR1A1A2(orf3)A3A4BCX0X1X2X3D, encoding the enzymes for conversion of biphenyl to acetyl coenzyme A. In this study, the salicylate-catabolic (sal) gene cluster encoding the enzymes for conversion of salicylate to acetyl coenzyme A were identified 6.6-kb downstream of the bph gene cluster along with a second regulatory gene, bphR2. Both the bph and sal genes were cross-regulated positively and/or negatively by the two regulatory proteins, BphR1 and BphR2, in the presence or absence of the effectors. The BphR2 binding sequence exhibits homology with the NahR binding sequences in various naphthalene-degrading bacteria. Based on previous studies and the present study we propose a new regulatory model for biphenyl and salicylate catabolism in strain KF707. 10.1128/JB.00329-06</description>
    <dc:title>Cross-Regulation of Biphenyl- and Salicylate-Catabolic Genes by Two Regulatory Systems in Pseudomonas pseudoalcaligenes KF707</dc:title>

    <dc:creator>Hidehiko Fujihara</dc:creator>
    <dc:creator>Hideyuki Yoshida</dc:creator>
    <dc:creator>Tetsuya Matsunaga</dc:creator>
    <dc:creator>Masatoshi Goto</dc:creator>
    <dc:creator>Kensuke Furukawa</dc:creator>
    <dc:identifier>doi:10.1128/JB.00329-06</dc:identifier>
    <dc:source>J. Bacteriol., Vol. 188, No. 13. (1 July 2006), pp. 4690-4697.</dc:source>
    <dc:date>2008-07-16T17:10:29-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>J. Bacteriol.</prism:publicationName>
    <prism:volume>188</prism:volume>
    <prism:number>13</prism:number>
    <prism:startingPage>4690</prism:startingPage>
    <prism:endingPage>4697</prism:endingPage>
    <prism:category>biodegradation</prism:category>
    <prism:category>cross-regulation</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/TheresaNiederberger/article/2102204">
    <title>KEGG for linking genomes to life and the environment</title>
    <link>http://www.citeulike.org/user/TheresaNiederberger/article/2102204</link>
    <description>&lt;i&gt;Nucl. Acids Res. (12 December 2007), gkm882.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;KEGG (http://www.genome.jp/kegg/) is a database of biological systems that integrates genomic, chemical and systemic functional information. KEGG provides a reference knowledge base for linking genomes to life through the process of PATHWAY mapping, which is to map, for example, a genomic or transcriptomic content of genes to KEGG reference pathways to infer systemic behaviors of the cell or the organism. In addition, KEGG provides a reference knowledge base for linking genomes to the environment, such as for the analysis of drug-target relationships, through the process of BRITE mapping. KEGG BRITE is an ontology database representing functional hierarchies of various biological objects, including molecules, cells, organisms, diseases and drugs, as well as relationships among them. KEGG PATHWAY is now supplemented with a new global map of metabolic pathways, which is essentially a combined map of about 120 existing pathway maps. In addition, smaller pathway modules are defined and stored in KEGG MODULE that also contains other functional units and complexes. The KEGG resource is being expanded to suit the needs for practical applications. KEGG DRUG contains all approved drugs in the US and Japan, and KEGG DISEASE is a new database linking disease genes, pathways, drugs and diagnostic markers. 10.1093/nar/gkm882</description>
    <dc:title>KEGG for linking genomes to life and the environment</dc:title>

    <dc:creator>Minoru Kanehisa</dc:creator>
    <dc:creator>Michihiro Araki</dc:creator>
    <dc:creator>Susumu Goto</dc:creator>
    <dc:creator>Masahiro Hattori</dc:creator>
    <dc:creator>Mika Hirakawa</dc:creator>
    <dc:creator>Masumi Itoh</dc:creator>
    <dc:creator>Toshiaki Katayama</dc:creator>
    <dc:creator>Shuichi Kawashima</dc:creator>
    <dc:creator>Shujiro Okuda</dc:creator>
    <dc:creator>Toshiaki Tokimatsu</dc:creator>
    <dc:creator>Yoshihiro Yamanishi</dc:creator>
    <dc:identifier>doi:10.1093/nar/gkm882</dc:identifier>
    <dc:source>Nucl. Acids Res. (12 December 2007), gkm882.</dc:source>
    <dc:date>2007-12-13T06:01:37-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Nucl. Acids Res.</prism:publicationName>
    <prism:startingPage>gkm882</prism:startingPage>
    <prism:category>diplomarbeit</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/mmuecke/article/2952250">
    <title>Anatomy of high-performance matrix multiplication</title>
    <link>http://www.citeulike.org/user/mmuecke/article/2952250</link>
    <description>&lt;i&gt;ACM Trans. Math. Softw., Vol. 34, No. 3. (May 2008), pp. 1-25.&lt;/i&gt;</description>
    <dc:title>Anatomy of high-performance matrix multiplication</dc:title>

    <dc:creator>Kazushige Goto</dc:creator>
    <dc:creator>Robert van de Geijn</dc:creator>
    <dc:identifier>doi:10.1145/1356052.1356053</dc:identifier>
    <dc:source>ACM Trans. Math. Softw., Vol. 34, No. 3. (May 2008), pp. 1-25.</dc:source>
    <dc:date>2008-07-02T13:49:21-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>ACM Trans. Math. Softw.</prism:publicationName>
    <prism:issn>0098-3500</prism:issn>
    <prism:volume>34</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>1</prism:startingPage>
    <prism:endingPage>25</prism:endingPage>
    <prism:publisher>ACM</prism:publisher>
    <prism:category>high-performance_computing</prism:category>
    <prism:category>sparse_matrix</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/pulsus-morbi/article/2951663">
    <title>Formation of dense partonic matter in relativistic nucleus-nucleus collisions at RHIC: Experimental evaluation by the PHENIX Collaboration</title>
    <link>http://www.citeulike.org/user/pulsus-morbi/article/2951663</link>
    <description>&lt;i&gt;Nuclear Physics A, Vol. 757, No. 1-2. (8 August 2005), pp. 184-283.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Extensive experimental data from high-energy nucleus-nucleus collisions were recorded using the PHENIX detector at the Relativistic Heavy Ion Collider (RHIC). The comprehensive set of measurements from the first three years of RHIC operation includes charged particle multiplicities, transverse energy, yield ratios and spectra of identified hadrons in a wide range of transverse momenta (pT), elliptic flow, two-particle correlations, nonstatistical fluctuations, and suppression of particle production at high pT. The results are examined with an emphasis on implications for the formation of a new state of dense matter. We find that the state of matter created at RHIC cannot be described in terms of ordinary color neutral hadrons.</description>
    <dc:title>Formation of dense partonic matter in relativistic nucleus-nucleus collisions at RHIC: Experimental evaluation by the PHENIX Collaboration</dc:title>

    <dc:creator>K Adcox</dc:creator>
    <dc:creator>Phenix-Collaboration</dc:creator>
    <dc:identifier>doi:10.1016/j.nuclphysa.2005.03.086</dc:identifier>
    <dc:source>Nuclear Physics A, Vol. 757, No. 1-2. (8 August 2005), pp. 184-283.</dc:source>
    <dc:date>2008-07-02T09:39:16-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Nuclear Physics A</prism:publicationName>
    <prism:volume>757</prism:volume>
    <prism:number>1-2</prism:number>
    <prism:startingPage>184</prism:startingPage>
    <prism:endingPage>283</prism:endingPage>
    <prism:category>experimentalist</prism:category>
    <prism:category>jet</prism:category>
    <prism:category>supresssion</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/natstreet/article/454582">
    <title>From genomics to chemical genomics: new developments in KEGG.</title>
    <link>http://www.citeulike.org/user/natstreet/article/454582</link>
    <description>&lt;i&gt;Nucleic Acids Res, Vol. 34, No. Database issue. (1 January 2006), pp. 354-357.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The increasing amount of genomic and molecular information is the basis for understanding higher-order biological systems, such as the cell and the organism, and their interactions with the environment, as well as for medical, industrial and other practical applications. The KEGG resource (http://www.genome.jp/kegg/) provides a reference knowledge base for linking genomes to biological systems, categorized as building blocks in the genomic space (KEGG GENES) and the chemical space (KEGG LIGAND), and wiring diagrams of interaction networks and reaction networks (KEGG PATHWAY). A fourth component, KEGG BRITE, has been formally added to the KEGG suite of databases. This reflects our attempt to computerize functional interpretations as part of the pathway reconstruction process based on the hierarchically structured knowledge about the genomic, chemical and network spaces. In accordance with the new chemical genomics initiatives, the scope of KEGG LIGAND has been significantly expanded to cover both endogenous and exogenous molecules. Specifically, RPAIR contains curated chemical structure transformation patterns extracted from known enzymatic reactions, which would enable analysis of genome-environment interactions, such as the prediction of new reactions and new enzyme genes that would degrade new environmental compounds. Additionally, drug information is now stored separately and linked to new KEGG DRUG structure maps.</description>
    <dc:title>From genomics to chemical genomics: new developments in KEGG.</dc:title>

    <dc:creator>M Kanehisa</dc:creator>
    <dc:creator>S Goto</dc:creator>
    <dc:creator>M Hattori</dc:creator>
    <dc:creator>KF Aoki-Kinoshita</dc:creator>
    <dc:creator>M Itoh</dc:creator>
    <dc:creator>S Kawashima</dc:creator>
    <dc:creator>T Katayama</dc:creator>
    <dc:creator>M Araki</dc:creator>
    <dc:creator>M Hirakawa</dc:creator>
    <dc:source>Nucleic Acids Res, Vol. 34, No. Database issue. (1 January 2006), pp. 354-357.</dc:source>
    <dc:date>2006-01-02T20:24:29-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Nucleic Acids Res</prism:publicationName>
    <prism:issn>1362-4962</prism:issn>
    <prism:volume>34</prism:volume>
    <prism:number>Database issue</prism:number>
    <prism:startingPage>354</prism:startingPage>
    <prism:endingPage>357</prism:endingPage>
    <prism:category>popgenie-ms</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/sim82/article/771675">
    <title>LIGAND: database of chemical compounds and reactions in biological pathways.</title>
    <link>http://www.citeulike.org/user/sim82/article/771675</link>
    <description>&lt;i&gt;Nucleic Acids Res, Vol. 30, No. 1. (1 January 2002), pp. 402-404.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;LIGAND is a composite database comprising three sections: COMPOUND for the information about metabolites and other chemical compounds, REACTION for the collection of substrate-product relations representing metabolic and other reactions, and ENZYME for the information about enzyme molecules. The current release (as of September 7, 2001) includes 7298 compounds, 5166 reactions and 3829 enzymes. In addition to the keyword search provided by the DBGET/LinkDB system, a substructure search to the COMPOUND and REACTION sections is now available through the World Wide Web (http://www.genome.ad.jp/ligand/). LIGAND may be also downloaded by anonymous FTP (ftp://ftp.genome.ad.jp/pub/kegg/ligand/).</description>
    <dc:title>LIGAND: database of chemical compounds and reactions in biological pathways.</dc:title>

    <dc:creator>S Goto</dc:creator>
    <dc:creator>Y Okuno</dc:creator>
    <dc:creator>M Hattori</dc:creator>
    <dc:creator>T Nishioka</dc:creator>
    <dc:creator>M Kanehisa</dc:creator>
    <dc:identifier>doi:10.1093/nar/30.1.402</dc:identifier>
    <dc:source>Nucleic Acids Res, Vol. 30, No. 1. (1 January 2002), pp. 402-404.</dc:source>
    <dc:date>2006-07-24T17:44:14-00:00</dc:date>
    <prism:publicationYear>2002</prism:publicationYear>
    <prism:publicationName>Nucleic Acids Res</prism:publicationName>
    <prism:issn>1362-4962</prism:issn>
    <prism:volume>30</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>402</prism:startingPage>
    <prism:endingPage>404</prism:endingPage>
    <prism:category>database</prism:category>
    <prism:category>kegg</prism:category>
    <prism:category>reaction</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/shoshin/article/2937921">
    <title>Prefrontal Cortical Synaptic Plasticity: The Roles of Dopamine and Implication for Schizophrenia</title>
    <link>http://www.citeulike.org/user/shoshin/article/2937921</link>
    <description>&lt;i&gt;Monoaminergic Modulation of Cortical Excitability (2007), pp. 165-174.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The prefrontal cortex (PFC) is central in mediating executive functions in goaldirected behavior, for which proper dopamine (DA) actions of information processing modulation is essential in this area. It is now evident that, as in the case of the hippocampus, the PFC undergoes neuronal adaptation processes in its networks with induction of synaptic plasticity such as long-term potentiation (LTP) and short-term potentiation (STP). A prominent characteristic of synaptic plasticity in the PFC is that its induction mechanisms involve DA as an essential modulatory molecule. As such, DA-dependent plastic changes occurring in PFC network have important roles for PFC-mediated cognitive functions. Nevertheless, little attempt has been made to characterize the nature of PFC neuronal adaptation by synaptic plasticity, given that the PFC is thought to be the area of temporary storage and manipulation of information, known as working memory. However, accumulating evidences now indicate that the functions of the PFC cannot be fully explained just as the region of an online representation and handling of information. Importance of DA-dependent synaptic plasticity is further encouraged by possible disruption of synaptic plasticity mechanism in the PFC in psychiatric disorders such as schizophrenia, drug addiction, and depression. In this chapter, we describe the underlying cellular mechanisms of DA action on synaptic plasticity induction in the PFC, and possible roles of PFC synaptic plasticity in executive functions as well as its disruptions in the pathophysiology of schizophrenia.</description>
    <dc:title>Prefrontal Cortical Synaptic Plasticity: The Roles of Dopamine and Implication for Schizophrenia</dc:title>

    <dc:creator>Yukiori Goto</dc:creator>
    <dc:creator>Satoru Otani</dc:creator>
    <dc:identifier>doi:10.1007/978-0-387-72256-6_10</dc:identifier>
    <dc:source>Monoaminergic Modulation of Cortical Excitability (2007), pp. 165-174.</dc:source>
    <dc:date>2008-06-27T18:48:06-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Monoaminergic Modulation of Cortical Excitability</prism:publicationName>
    <prism:startingPage>165</prism:startingPage>
    <prism:endingPage>174</prism:endingPage>
    <prism:category>attention</prism:category>
    <prism:category>dopamine</prism:category>
    <prism:category>gamma_band</prism:category>
    <prism:category>networks</prism:category>
    <prism:category>plasticity</prism:category>
    <prism:category>prefrontal_cortex</prism:category>
    <prism:category>synchrony</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/ccsmith/article/2931410">
    <title>A reconfigurable adaptive FEC system for reliable wireless communications</title>
    <link>http://www.citeulike.org/user/ccsmith/article/2931410</link>
    <description>&lt;i&gt;Circuits and Systems, 2004. Proceedings. The 2004 IEEE Asia-Pacific Conference on, Vol. 1 (2004), pp. 13-16 vol.1.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;This work proposes a reconfigurable adaptive FEC system. For adaptive FEC schemes, we can implement an FEC decoder which is optimal for error correction capability (t) by taking the number of operations into consideration. Reconfiguring the optimal FEC decoder dynamically for each t allows us to maximize the throughput of each decoder within a limited hardware resource. Our system can reduce packet dropping rate more efficiently than conventional fixed hardware systems for a reliable transport protocol.</description>
    <dc:title>A reconfigurable adaptive FEC system for reliable wireless communications</dc:title>

    <dc:creator>K Shimizu</dc:creator>
    <dc:creator>N Togawa</dc:creator>
    <dc:creator>T Ikenaga</dc:creator>
    <dc:creator>M Yanagisawa</dc:creator>
    <dc:creator>S Goto</dc:creator>
    <dc:creator>T Ohtsuki</dc:creator>
    <dc:identifier>doi:10.1109/APCCAS.2004.1412679</dc:identifier>
    <dc:source>Circuits and Systems, 2004. Proceedings. The 2004 IEEE Asia-Pacific Conference on, Vol. 1 (2004), pp. 13-16 vol.1.</dc:source>
    <dc:date>2008-06-26T16:20:02-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>Circuits and Systems, 2004. Proceedings. The 2004 IEEE Asia-Pacific Conference on</prism:publicationName>
    <prism:volume>1</prism:volume>
    <prism:startingPage>13</prism:startingPage>
    <prism:endingPage>16 vol.1</prism:endingPage>
    <prism:category>adhoc</prism:category>
    <prism:category>network</prism:category>
    <prism:category>tcp_vgrid</prism:category>
    <prism:category>transport</prism:category>
    <prism:category>vehicular</prism:category>
    <prism:category>wireless</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/carlk/article/1397177">
    <title>The commonality of protein interaction networks determined in Neurodegenerative disorders (NDDs).</title>
    <link>http://www.citeulike.org/user/carlk/article/1397177</link>
    <description>&lt;i&gt;Bioinformatics (6 June 2007)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;MOTIVATION: Neurodegenerative disorders (NDDs) are progressive and fatal disorders, which are commonly characterized by the intracellular or extracellular presence of abnormal protein aggregates. The identification and verification of proteins interacting with causative gene products are effective ways to understand their physiological and pathological functions. The objective of this research is to better understand common molecular pathogenic mechanisms in NDDs by employing protein-protein interaction networks, the domain characteristics commonly identified in NDDs and correlation among NDDs based on domain information. RESULTS: By reviewing published literatures in PubMed, we created pathway maps in Kyoto Encyclopedia of Genes and Genomes (KEGG) for the protein-protein interactions in six NDDs: Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), dentatorubral-pallidoluysian atrophy (DRPLA) and prion disease (PRION). We also collected data on 201 interacting proteins and 13 compounds with 282 interactions from the literature. We found 19 proteins common to these six NDDs. These common proteins were mainly involved in the apoptosis and MAPK signaling pathways. We expanded the interaction network by adding protein interaction data from the Human Protein Reference Database and gene expression data from the Human Gene Expression Index Database. We then carried out domain analysis on the extended network and found the characteristic domains, such as 14-3-3 protein, phosphotyrosine interaction domain and caspase domain, for the common proteins. Moreover, we found a relatively high correlation between AD, PD, HD and PRION, but not ALS or DRPLA, in terms of the protein domain distributions. AVAILABILITY: http://www.genome.jp/kegg/pathway/hsa/hsa01510.html (KEGG pathway maps for NDDs).</description>
    <dc:title>The commonality of protein interaction networks determined in Neurodegenerative disorders (NDDs).</dc:title>

    <dc:creator>Vachiranee Limviphuvadh</dc:creator>
    <dc:creator>Seigo Tanaka</dc:creator>
    <dc:creator>Susumu Goto</dc:creator>
    <dc:creator>Kunihiro Ueda</dc:creator>
    <dc:creator>Minoru Kanehisa</dc:creator>
    <dc:identifier>doi:10.1093/bioinformatics/btm307</dc:identifier>
    <dc:source>Bioinformatics (6 June 2007)</dc:source>
    <dc:date>2007-06-18T15:19:17-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Bioinformatics</prism:publicationName>
    <prism:issn>1460-2059</prism:issn>
    <prism:category>comparison</prism:category>
    <prism:category>disease</prism:category>
    <prism:category>networks</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/marcio/article/2873406">
    <title>Long-range negative correlation of glucose dynamics in humans and its breakdown in diabetes mellitus</title>
    <link>http://www.citeulike.org/user/marcio/article/2873406</link>
    <description>&lt;i&gt;Am J Physiol Regul Integr Comp Physiol, Vol. 291, No. 6. (1 December 2006), pp. R1638-1643.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Diurnal fluctuations in glucose levels continuously monitored during normal daily life are investigated using an extended random walk analysis, referred to as detrended fluctuation analysis (DFA), in 12 nondiabetic subjects and 15 diabetic patients. The DFA exponent alpha = 1.25 +/- 0.29 for healthy individuals in the &#34;long-range&#34; (&#62;2 h) regime is shown to be significantly (P &#60; 0.01) smaller than the reference &#34;uncorrelated&#34; value of alpha = 1.5, suggesting that the instantaneous net effects of the dynamical balance of glucose flux and reflux, causing temporal changes in glucose concentration, are long-range negatively correlated. By contrast, in diabetic patients, the DFA exponent alpha = 1.65 +/- 0.30 is significantly (P &#60; 0.05) higher than that in nondiabetic subjects, evidencing a breakdown of the long-range negative correlation. It is suggested that the emergence of such positive long-range glucose correlations in diabetic patients--indicating that the net effects of the flux and reflux persist for many hours--likely reflects pathogenic mechanisms of diabetes, i.e., the lack of long-term stability of blood glucose and that the long-range negatively correlated glucose dynamics are functional in maintaining normal glucose homeostasis. 10.1152/ajpregu.00241.2006</description>
    <dc:title>Long-range negative correlation of glucose dynamics in humans and its breakdown in diabetes mellitus</dc:title>

    <dc:creator>Hitomi Ogata</dc:creator>
    <dc:creator>Kumpei Tokuyama</dc:creator>
    <dc:creator>Shoichiro Nagasaka</dc:creator>
    <dc:creator>Akihiko Ando</dc:creator>
    <dc:creator>Ikuyo Kusaka</dc:creator>
    <dc:creator>Naoko Sato</dc:creator>
    <dc:creator>Akiko Goto</dc:creator>
    <dc:creator>Shun Ishibashi</dc:creator>
    <dc:creator>Ken Kiyono</dc:creator>
    <dc:creator>Zbigniew Struzik</dc:creator>
    <dc:creator>Yoshiharu Yamamoto</dc:creator>
    <dc:identifier>doi:10.1152/ajpregu.00241.2006</dc:identifier>
    <dc:source>Am J Physiol Regul Integr Comp Physiol, Vol. 291, No. 6. (1 December 2006), pp. R1638-1643.</dc:source>
    <dc:date>2008-06-08T11:57:40-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Am J Physiol Regul Integr Comp Physiol</prism:publicationName>
    <prism:volume>291</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>R1638</prism:startingPage>
    <prism:endingPage>1643</prism:endingPage>
    <prism:category>dfa</prism:category>
    <prism:category>diabetes</prism:category>
    <prism:category>physiology</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/group/88/article/2869922">
    <title>Structure and Properties of High-Density Polymer Brushes Prepared by Surface-Initiated Living Radical Polymerization</title>
    <link>http://www.citeulike.org/group/88/article/2869922</link>
    <description>&lt;i&gt;Surface-Initiated Polymerization I (2006), pp. 1-45.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Surface modifications by polymers are becoming increasingly important for various applications ranging from biotechnology to advanced microelectronics. Recent successful applications of living radical polymerization (LRP) made it possible to graft various low-polydispersity polymers including simple homopolymers, end-functionalized polymers, block/random/gradient copolymers, and functional polymers. At the same time, this technique has brought about a striking increase of graft density. Graft chains in such a high-density polymer brush were found to be highly extended in good solvent, even to the order of their full lengths. It was also found that a high-density polymer brush has characteristic properties, in both swollen and dry states, quite different and unpredictable from those of the semi-dilute or moderately dense polymer brushes previously studied. This review highlights the recent development of surface-initiated LRP and the structures, properties, and potential applications of thereby obtainable high-density polymer brushes. It is believed that surface-initiated LRP is opening up a new route to “precision” surface modification.</description>
    <dc:title>Structure and Properties of High-Density Polymer Brushes Prepared by Surface-Initiated Living Radical Polymerization</dc:title>

    <dc:creator>Yoshinobu Tsujii</dc:creator>
    <dc:creator>Kohji Ohno</dc:creator>
    <dc:creator>Shinpei Yamamoto</dc:creator>
    <dc:creator>Atsushi Goto</dc:creator>
    <dc:creator>Takeshi Fukuda</dc:creator>
    <dc:identifier>doi:10.1007/12_063</dc:identifier>
    <dc:source>Surface-Initiated Polymerization I (2006), pp. 1-45.</dc:source>
    <dc:date>2008-06-06T15:28:21-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Surface-Initiated Polymerization I</prism:publicationName>
    <prism:startingPage>1</prism:startingPage>
    <prism:endingPage>45</prism:endingPage>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/kas/article/2869362">
    <title>Gate control of spin transport in multilayer graphene</title>
    <link>http://www.citeulike.org/user/kas/article/2869362</link>
    <description>&lt;i&gt;Applied Physics Letters, Vol. 92, No. 21. (2008)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;We experimentally studied the gate voltage dependence of spin transport in multilayer graphene (MLG) using the nonlocal spin detection technique. We found that the spin signal is a monotonically decreasing linear function of the resistance of MLG, which is characteristic of the intermediate interfacial transparency between the MLG and the ferromagnetic electrodes (Co). The linear relation indicates a large spin relaxation length significantly exceeding 8&#160;&#160;&#181;m. This shows the superiority of MLG for the utilization of the graphite-based spintronic devices. &#169;2008 American Institute of Physics</description>
    <dc:title>Gate control of spin transport in multilayer graphene</dc:title>

    <dc:creator>H Goto</dc:creator>
    <dc:creator>A Kanda</dc:creator>
    <dc:creator>T Sato</dc:creator>
    <dc:creator>S Tanaka</dc:creator>
    <dc:creator>Y Ootuka</dc:creator>
    <dc:creator>S Odaka</dc:creator>
    <dc:creator>H Miyazaki</dc:creator>
    <dc:creator>K Tsukagoshi</dc:creator>
    <dc:creator>Y Aoyagi</dc:creator>
    <dc:identifier>doi:10.1063/1.2937836</dc:identifier>
    <dc:source>Applied Physics Letters, Vol. 92, No. 21. (2008)</dc:source>
    <dc:date>2008-06-06T12:58:36-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Applied Physics Letters</prism:publicationName>
    <prism:volume>92</prism:volume>
    <prism:number>21</prism:number>
    <prism:publisher>AIP</prism:publisher>
    <prism:category>experimental</prism:category>
    <prism:category>graphene</prism:category>
    <prism:category>multilayer</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/sebastien_vigneau/article/2853762">
    <title>Maternally inherited X chromosome is not inactivated in mouse blastocysts due to parental imprinting.</title>
    <link>http://www.citeulike.org/user/sebastien_vigneau/article/2853762</link>
    <description>&lt;i&gt;Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology, Vol. 8, No. 2. (2000), pp. 101-109.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Mouse embryos having an additional maternally inherited X chromosome (X(M)) invariably die before midgestation with the deficient extraembryonic ectoderm of the polar trophectoderm lineage, whereas postnatal mice having an additional paternally inherited X chromosome (X(P)) survive beyond parturition. A cytogenetic study led us to hypothesize that abnormal development of such embryos disomic for X(M) (DsX(M)) is attributable to two doses of active X(M) chromosome in extraembryonic tissues. To test the validity of this hypothesis, we examined the initial X chromosome inactivation pattern in embryos at the blastocyst stage by means of replication banding method as well as RNA FISH detecting Xist transcripts. X(P) was the only asynchronously replicating X chromosome, if any, in X(M)X(M)X(P) blastocysts, and no such allocyclic X chromosome was ever detected in X(M)X(M)Y blastocysts. In agreement with these findings, only one Xist paint signal was detected in 79% of X(M)X(M)X(P) cells, whereas no such signal was found in X(M)X(M)Y embryos. Thus, the present study supports the hypothesis that two X chromosomes remaining active in the extraembryonic cell lineages due to the maternal imprinting explain the underdevelopment of extraembryonic structures and hence early postimplantation death of DsX(M) embryos.</description>
    <dc:title>Maternally inherited X chromosome is not inactivated in mouse blastocysts due to parental imprinting.</dc:title>

    <dc:creator>Y Goto</dc:creator>
    <dc:creator>N Takagi</dc:creator>
    <dc:source>Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology, Vol. 8, No. 2. (2000), pp. 101-109.</dc:source>
    <dc:date>2008-05-31T23:44:58-00:00</dc:date>
    <prism:publicationYear>2000</prism:publicationYear>
    <prism:publicationName>Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology</prism:publicationName>
    <prism:issn>0967-3849</prism:issn>
    <prism:volume>8</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>101</prism:startingPage>
    <prism:endingPage>109</prism:endingPage>
    <prism:category>imprint</prism:category>
    <prism:category>imprinting</prism:category>
    <prism:category>inactivation</prism:category>
    <prism:category>x-chromosome</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/l-alex/article/2853663">
    <title>A physical mechanism of the energy cascade in homogeneous isotropic turbulence</title>
    <link>http://www.citeulike.org/user/l-alex/article/2853663</link>
    <description>&lt;i&gt;Journal of Fluid Mechanics, Vol. 605, No. -1. (2008), pp. 355-366.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;In order to investigate the physical mechanism of the energy cascade in homogeneous isotropic turbulence, the internal energy and its transfer rate are defined as a function of scale, space and time. Direct numerical simulation of turbulence at a moderate Reynolds number verifies that the energy cascade can be caused by the successive creation of smaller-scale tubular vortices in the larger-scale straining regions existing between pairs of larger-scale tubular vortices. Movies are available with the online version of the paper.</description>
    <dc:title>A physical mechanism of the energy cascade in homogeneous isotropic turbulence</dc:title>

    <dc:creator>Susumu Goto</dc:creator>
    <dc:source>Journal of Fluid Mechanics, Vol. 605, No. -1. (2008), pp. 355-366.</dc:source>
    <dc:date>2008-05-31T20:47:51-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Journal of Fluid Mechanics</prism:publicationName>
    <prism:volume>605</prism:volume>
    <prism:number>-1</prism:number>
    <prism:startingPage>355</prism:startingPage>
    <prism:endingPage>366</prism:endingPage>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/krishlk/article/2853260">
    <title>POP method: an approach to enhance the security and privacy of RFID systems used in product lifecycle with an anonymous ownership transferring mechanism</title>
    <link>http://www.citeulike.org/user/krishlk/article/2853260</link>
    <description>&lt;i&gt;(2007), pp. 270-275.&lt;/i&gt;</description>
    <dc:title>POP method: an approach to enhance the security and privacy of RFID systems used in product lifecycle with an anonymous ownership transferring mechanism</dc:title>

    <dc:creator>Sabaragamu Koralalage</dc:creator>
    <dc:creator>Mohammed Reza</dc:creator>
    <dc:creator>J Miura</dc:creator>
    <dc:creator>Y Goto</dc:creator>
    <dc:creator>J Cheng</dc:creator>
    <dc:identifier>doi:10.1145/1244002.1244069</dc:identifier>
    <dc:source>(2007), pp. 270-275.</dc:source>
    <dc:date>2008-05-31T14:19:30-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:startingPage>270</prism:startingPage>
    <prism:endingPage>275</prism:endingPage>
    <prism:publisher>ACM</prism:publisher>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/gaber/article/2851107">
    <title>The Cassiopeia A Supernova was of Type IIB</title>
    <link>http://www.citeulike.org/user/gaber/article/2851107</link>
    <description>&lt;i&gt;(29 May 2008)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Cassiopeia A is one of the youngest supernova remnants known in the Milky Way and a unique laboratory for supernova physics. We present an optical spectrum of the Cassiopeia A supernova near maximum brightness, obtained from observations of a scattered light echo - more than three centuries after the direct light of the explosion swept past Earth. The spectrum shows that Cassiopeia A was a type IIb supernova and originated from the collapse of the helium core of a red supergiant that had lost most of its hydrogen envelope prior to exploding. Our finding concludes a longstanding debate on the Cassiopeia A progenitor and provides new insight into supernova physics by linking the properties of the explosion to the wealth of knowledge about its remnant.</description>
    <dc:title>The Cassiopeia A Supernova was of Type IIB</dc:title>

    <dc:creator>Oliver Krause</dc:creator>
    <dc:creator>Stephan Birkmann</dc:creator>
    <dc:creator>Tomonori Usuda</dc:creator>
    <dc:creator>Takashi Hattori</dc:creator>
    <dc:creator>Miwa Goto</dc:creator>
    <dc:creator>George Rieke</dc:creator>
    <dc:creator>Karl Misselt</dc:creator>
    <dc:source>(29 May 2008)</dc:source>
    <dc:date>2008-05-30T22:37:18-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:category>observations</prism:category>
    <prism:category>supernova</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jyuh/article/2846149">
    <title>APPLICATION OF AN ADENOVIRAL VECTOR ENCODING SOLUBLE TRANSFORMING GROWTH FACTOR-beta TYPE II RECEPTOR TO THE TREATMENT OF DIABETIC NEPHROPATHY IN MICE.</title>
    <link>http://www.citeulike.org/user/jyuh/article/2846149</link>
    <description>&lt;i&gt;Clinical and experimental pharmacology &#38; physiology (23 May 2008)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;1. In the present study, we examined the effects of inhibiting transforming growth factor (TGF)-beta in a mouse model of diabetic nephropathy. 2. An adenovirus harbouring the gene encoding soluble TGF-beta type II receptor (Ad.CAG-sTbetaRII), a competitive inhibitor of TGF-beta, was injected into hindlimb muscles (systemic delivery) of mice 5 weeks after the induction of diabetes with streptozotocin. The control group was injected with an adenovirus encoding the LacZ gene (Ad-LacZ). 3. Five weeks after administration, anti-TGF-beta gene therapy was found to have had no effect on renal function, albuminuria or glucose metabolism in mice with diabetic nephropathy. Nonetheless, this gene therapy did significantly reduce fibrosis in both glomeruli and renal tubules. These effects were accompanied by attenuation of the increased expression of alpha-smooth muscle actin normally seen in kidneys of diabetic mice and better preservation of glomerular cell numbers, although the thickness of the glomerular capillary basement membrane was unchanged. The plasma concentration of soluble TGF-beta type II receptor peaked on Day 7 after treatment, but was undetectable by Day 14. Moreover, a second treatment with Ad.CAG-sTbetaRII failed to prolong the interval of gene product expression in the blood. 4. The present anti-TGF-beta gene therapy showed a significant antifibrotic effect in a model of diabetic nephropathy, but failed to improve renal function. The inadequacy of the observed effect is likely due to the relatively short interval of gene product expression. This problem will have to be overcome if gene therapies for slowly progressing diseases, like diabetic nephropathy, are to be realised.</description>
    <dc:title>APPLICATION OF AN ADENOVIRAL VECTOR ENCODING SOLUBLE TRANSFORMING GROWTH FACTOR-beta TYPE II RECEPTOR TO THE TREATMENT OF DIABETIC NEPHROPATHY IN MICE.</dc:title>

    <dc:creator>Takehito Kondo</dc:creator>
    <dc:creator>Genzou Takemura</dc:creator>
    <dc:creator>Ken-Ichiro Kosai</dc:creator>
    <dc:creator>Takamasa Ohno</dc:creator>
    <dc:creator>Tomoyuki Takahashi</dc:creator>
    <dc:creator>Masayasu Esaki</dc:creator>
    <dc:creator>Kazuko Goto</dc:creator>
    <dc:creator>Rumi Maruyama</dc:creator>
    <dc:creator>Ichijiro Murata</dc:creator>
    <dc:creator>Shinya Minatoguchi</dc:creator>
    <dc:creator>Takako Fujiwara</dc:creator>
    <dc:creator>Hisayoshi Fujiwara</dc:creator>
    <dc:identifier>doi:10.1111/j.1440-1681.2008.04967.x</dc:identifier>
    <dc:source>Clinical and experimental pharmacology &#38; physiology (23 May 2008)</dc:source>
    <dc:date>2008-05-30T02:49:50-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Clinical and experimental pharmacology &#38; physiology</prism:publicationName>
    <prism:issn>1440-1681</prism:issn>
    <prism:category>dn</prism:category>
    <prism:category>gene-therapy</prism:category>
    <prism:category>plasmid</prism:category>
    <prism:category>tgfb</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/srp33/article/1687719">
    <title>Combining microarrays and biological knowledge for estimating gene networks via Bayesian networks</title>
    <link>http://www.citeulike.org/user/srp33/article/1687719</link>
    <description>&lt;i&gt;Bioinformatics Conference, 2003. CSB 2003. Proceedings of the 2003 IEEE (2003), pp. 104-113.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;We propose a statistical method for estimating a gene network based on Bayesian networks from microarray gene expression data together with biological knowledge including protein-protein interactions, protein-DNA interactions, binding site information, existing literature and so on. Unfortunately, microarray data do not contain enough information for constructing gene networks accurately in many cases. Our method adds biological knowledge to the estimation method of gene networks under a Bayesian statistical framework, and also controls the trade-off between microarray information and biological knowledge automatically. We conduct Monte Carlo simulations to show the effectiveness of the proposed method. We analyze Saccharomyces cerevisiae gene expression data as an application.</description>
    <dc:title>Combining microarrays and biological knowledge for estimating gene networks via Bayesian networks</dc:title>

    <dc:creator>S Imoto</dc:creator>
    <dc:creator>T Higuchi</dc:creator>
    <dc:creator>T Goto</dc:creator>
    <dc:creator>K Tashiro</dc:creator>
    <dc:creator>S Kuhara</dc:creator>
    <dc:creator>S Miyano</dc:creator>
    <dc:identifier>doi:10.1109/CSB.2003.1227309</dc:identifier>
    <dc:source>Bioinformatics Conference, 2003. CSB 2003. Proceedings of the 2003 IEEE (2003), pp. 104-113.</dc:source>
    <dc:date>2007-09-23T18:52:56-00:00</dc:date>
    <prism:publicationYear>2003</prism:publicationYear>
    <prism:publicationName>Bioinformatics Conference, 2003. CSB 2003. Proceedings of the 2003 IEEE</prism:publicationName>
    <prism:startingPage>104</prism:startingPage>
    <prism:endingPage>113</prism:endingPage>
    <prism:category>bayesian_networks</prism:category>
    <prism:category>prior_knowledge</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/ceegrs2/article/2827751">
    <title>High performance VLSI architecture of fractional motion estimation in H.264 for HDTV</title>
    <link>http://www.citeulike.org/user/ceegrs2/article/2827751</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;Fractional motion estimation (FME) on sub-pixels will occupy almost over 45% of the computation complexity of H.264 encoding process. Therefore a high performance VLSI architecture of FME is described in this paper to achieve the capacity of encoding the high-resolution real-time video stream for HDTV. Our design is improved from an existing work by involving a pipeline strategy in sub-pixel interpolation unit which can avoid the long delay paths in 6-tap ID FIR so as to increase the clock frequency up to 200MHz. Moreover, a 16-pixel search engine is adopted to remove the redundant interpolation area and parallelize the various block size search which can save more than half of the clock cycles in processing a macro block. Our design is implemented with only 189K gates at operating frequency of 200MHz in worst case (285MHz in typical case). It can provide the processing capacity of more than 250K MB/sec which is enough for 1080HD (1920/spl times/1088) video streams at frame rate of 30fps. It is a useful intellectual property (IP) design for multimedia system.</description>
    <dc:title>High performance VLSI architecture of fractional motion estimation in H.264 for HDTV</dc:title>

    <dc:creator>Changqi Yang</dc:creator>
    <dc:creator>S Goto</dc:creator>
    <dc:creator>T Ikenaga</dc:creator>
    <dc:identifier>doi:10.1109/ISCAS.2006.1693157</dc:identifier>
    <dc:source>Circuits and Systems, 2006. ISCAS 2006. Proceedings. 2006 IEEE International Symposium on (2006), 4 pp..</dc:source>
    <dc:date>2008-05-24T11:53:19-00:00</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>fractional</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Evangelia/article/2819817">
    <title>Rho-Kinase Phosphorylates PAR-3 and Disrupts PAR Complex Formation</title>
    <link>http://www.citeulike.org/user/Evangelia/article/2819817</link>
    <description>&lt;i&gt;Developmental Cell, Vol. 14, No. 2. (12 February 2008), pp. 205-215.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Summary A polarity complex of PAR-3, PAR-6, and atypical protein kinase C (aPKC) functions in various cell polarization events. PAR-3 directly interacts with Tiam1/Taim2 (STEF), Rac1-specific guanine nucleotide exchange factors, and forms a complex with aPKC-PAR-6-Cdc42-GTP, leading to Rac1 activation. RhoA antagonizes Rac1 in certain types of cells. However, the relationship between RhoA and the PAR complex remains elusive. We found here that Rho-kinase/ROCK/ROK, the effector of RhoA, phosphorylated PAR-3 at Thr833 and thereby disrupted its interaction with aPKC and PAR-6, but not with Tiam2. Phosphorylated PAR-3 was observed in the leading edge, and in central and rear portions of migrating cells having front-rear polarity. Knockdown of PAR-3 by small interfering RNA (siRNA) impaired cell migration, front-rear polarization, and PAR-3-mediated Rac1 activation, which were recovered with siRNA-resistant PAR-3, but not with the phospho-mimic PAR-3 mutant. We propose that RhoA/Rho-kinase inhibits PAR complex formation through PAR-3 phosphorylation, resulting in Rac1 inactivation.</description>
    <dc:title>Rho-Kinase Phosphorylates PAR-3 and Disrupts PAR Complex Formation</dc:title>

    <dc:creator>Masanori Nakayama</dc:creator>
    <dc:creator>Takaaki Goto</dc:creator>
    <dc:creator>Masayuki Sugimoto</dc:creator>
    <dc:creator>Takashi Nishimura</dc:creator>
    <dc:creator>Takafumi Shinagawa</dc:creator>
    <dc:creator>Sigeo Ohno</dc:creator>
    <dc:creator>Mutsuki Amano</dc:creator>
    <dc:creator>Kozo Kaibuchi</dc:creator>
    <dc:identifier>doi:10.1016/j.devcel.2007.11.021</dc:identifier>
    <dc:source>Developmental Cell, Vol. 14, No. 2. (12 February 2008), pp. 205-215.</dc:source>
    <dc:date>2008-05-21T12:59:51-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Developmental Cell</prism:publicationName>
    <prism:volume>14</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>205</prism:startingPage>
    <prism:endingPage>215</prism:endingPage>
    <prism:category>example</prism:category>
    <prism:category>experimental</prism:category>
    <prism:category>peptides</prism:category>
    <prism:category>phospho_peptides</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/deves/article/2815456">
    <title>A novel human insulinoma-associated cDNA, IA-1, encodes a protein with &#34;zinc-finger&#34; DNA-binding motifs.</title>
    <link>http://www.citeulike.org/user/deves/article/2815456</link>
    <description>&lt;i&gt;The Journal of biological chemistry, Vol. 267, No. 21. (25 July 1992), pp. 15252-15257.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;A subtraction library was constructed from human insulinoma (beta cell tumor) and glucagonoma (alpha cell tumor) cDNA phagemid libraries. Differential screening of 153 clones with end-labeled mRNAs from insulinoma, glucagonoma, and HeLa cells resulted in the isolation of a novel cDNA clone designated IA-1. This cDNA clone has a 2838-base pair sequence consisting of an open reading frame of 1530 nucleotides, which translates into a protein of 510 amino acids with a pI value of 9.1 and a molecular mass of 52,923 daltons. At the 3'-untranslated region there are seven ATTTA sequences between two polyadenylation signals (AATAAA). The IA-1 protein can be divided into two domains based upon the features of its amino acid sequence. The NH2-terminal domain of the deduced protein sequence (amino acids 1-250) has four classical pro-hormone dibasic conversion sites and an amidation signal sequence, Pro-Gly-Lys-Arg. The COOH-terminal domain (amino acids 251-510) contains five putative &#34;zinc-finger&#34; DNA-binding motifs of the form X3-Cys-X2-4-Cys-X12-His-X3-4-His-X4 which has been described as a consensus sequence for members of the Cys2-His2 DNA-binding protein class. Northern blot analysis revealed IA-1 mRNA in five of five human insulinoma and three of three murine insulinoma cell lines. Expression of this gene was undetectable in normal tissues. Additional tissue studies revealed that the message is expressed in several tumor cell lines of neuroendocrine origin including pheochromocytoma, medullary thyroid carcinoma, insulinoma, pituitary tumor, and small cell lung carcinoma. The restricted tissue distribution and unique sequence motifs suggest that this novel cDNA clone may encode a protein associated with the transformation of neuroendocrine cells.</description>
    <dc:title>A novel human insulinoma-associated cDNA, IA-1, encodes a protein with &#34;zinc-finger&#34; DNA-binding motifs.</dc:title>

    <dc:creator>Y Goto</dc:creator>
    <dc:creator>MG De Silva</dc:creator>
    <dc:creator>A Toscani</dc:creator>
    <dc:creator>BS Prabhakar</dc:creator>
    <dc:creator>AL Notkins</dc:creator>
    <dc:creator>MS Lan</dc:creator>
    <dc:source>The Journal of biological chemistry, Vol. 267, No. 21. (25 July 1992), pp. 15252-15257.</dc:source>
    <dc:date>2008-05-20T09:25:35-00:00</dc:date>
    <prism:publicationYear>1992</prism:publicationYear>
    <prism:publicationName>The Journal of biological chemistry</prism:publicationName>
    <prism:issn>0021-9258</prism:issn>
    <prism:volume>267</prism:volume>
    <prism:number>21</prism:number>
    <prism:startingPage>15252</prism:startingPage>
    <prism:endingPage>15257</prism:endingPage>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jyuh/article/2341115">
    <title>Calcium, Phosphorus, Cardiovascular Events and All-cause Mortality in Hemodialysis Patients: A Single-center Retrospective Cohort Study to Reassess the Validity of the Japanese Society for Dialysis Therapy Guidelines</title>
    <link>http://www.citeulike.org/user/jyuh/article/2341115</link>
    <description>&lt;i&gt;Therapeutic Apheresis and Dialysis, Vol. 12, No. 1. (February 2008), pp. 42-48.&lt;/i&gt;</description>
    <dc:title>Calcium, Phosphorus, Cardiovascular Events and All-cause Mortality in Hemodialysis Patients: A Single-center Retrospective Cohort Study to Reassess the Validity of the Japanese Society for Dialysis Therapy Guidelines</dc:title>

    <dc:creator>Komaba</dc:creator>
    <dc:creator>Hirotaka</dc:creator>
    <dc:creator>Igaki</dc:creator>
    <dc:creator>Naoya</dc:creator>
    <dc:creator>Takashima</dc:creator>
    <dc:creator>Mototsugu</dc:creator>
    <dc:creator>Goto</dc:creator>
    <dc:creator>Shunsuke</dc:creator>
    <dc:creator>Yokota</dc:creator>
    <dc:creator>Kazuki</dc:creator>
    <dc:creator>Komada</dc:creator>
    <dc:creator>Hisako</dc:creator>
    <dc:creator>Takemoto</dc:creator>
    <dc:creator>Toshiyuki</dc:creator>
    <dc:creator>Kohno</dc:creator>
    <dc:creator>Maki</dc:creator>
    <dc:creator>Kadoguchi</dc:creator>
    <dc:creator>Hiraku</dc:creator>
    <dc:creator>Hirosue</dc:creator>
    <dc:creator>Yoshiaki</dc:creator>
    <dc:creator>Goto</dc:creator>
    <dc:creator>Takeo</dc:creator>
    <dc:identifier>doi:10.1111/j.1744-9987.2007.00539.x</dc:identifier>
    <dc:source>Therapeutic Apheresis and Dialysis, Vol. 12, No. 1. (February 2008), pp. 42-48.</dc:source>
    <dc:date>2008-02-06T12:34:36-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Therapeutic Apheresis and Dialysis</prism:publicationName>
    <prism:issn>1744-9979</prism:issn>
    <prism:volume>12</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>42</prism:startingPage>
    <prism:endingPage>48</prism:endingPage>
    <prism:publisher>Blackwell Publishing</prism:publisher>
    <prism:category>hd</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/shung/article/2785899">
    <title>A system for functional analysis of Ebola virus glycoprotein.</title>
    <link>http://www.citeulike.org/user/shung/article/2785899</link>
    <description>&lt;i&gt;Proceedings of the National Academy of Sciences of the United States of America, Vol. 94, No. 26. (23 December 1997), pp. 14764-14769.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Ebola virus causes hemorrhagic fever in humans and nonhuman primates, resulting in mortality rates of up to 90%. Studies of this virus have been hampered by its extraordinary pathogenicity, which requires biosafety level 4 containment. To circumvent this problem, we developed a novel complementation system for functional analysis of Ebola virus glycoproteins. It relies on a recombinant vesicular stomatitis virus (VSV) that contains the green fluorescent protein gene instead of the receptor-binding G protein gene (VSVDeltaG*). Herein we show that Ebola Reston virus glycoprotein (ResGP) is efficiently incorporated into VSV particles. This recombinant VSV with integrated ResGP (VSVDeltaG*-ResGP) infected primate cells more efficiently than any of the other mammalian or avian cells examined, in a manner consistent with the host range tropism of Ebola virus, whereas VSVDeltaG* complemented with VSV G protein (VSVDeltaG*-G) efficiently infected the majority of the cells tested. We also tested the utility of this system for investigating the cellular receptors for Ebola virus. Chemical modification of cells to alter their surface proteins markedly reduced their susceptibility to VSVDeltaG*-ResGP but not to VSVDeltaG*-G. These findings suggest that cell surface glycoproteins with N-linked oligosaccharide chains contribute to the entry of Ebola viruses, presumably acting as a specific receptor and/or cofactor for virus entry. Thus, our VSV system should be useful for investigating the functions of glycoproteins from highly pathogenic viruses or those incapable of being cultured in vitro.</description>
    <dc:title>A system for functional analysis of Ebola virus glycoprotein.</dc:title>

    <dc:creator>A Takada</dc:creator>
    <dc:creator>C Robison</dc:creator>
    <dc:creator>H Goto</dc:creator>
    <dc:creator>A Sanchez</dc:creator>
    <dc:creator>KG Murti</dc:creator>
    <dc:creator>MA Whitt</dc:creator>
    <dc:creator>Y Kawaoka</dc:creator>
    <dc:source>Proceedings of the National Academy of Sciences of the United States of America, Vol. 94, No. 26. (23 December 1997), pp. 14764-14769.</dc:source>
    <dc:date>2008-05-11T22:23:27-00:00</dc:date>
    <prism:publicationYear>1997</prism:publicationYear>
    <prism:publicationName>Proceedings of the National Academy of Sciences of the United States of America</prism:publicationName>
    <prism:issn>0027-8424</prism:issn>
    <prism:volume>94</prism:volume>
    <prism:number>26</prism:number>
    <prism:startingPage>14764</prism:startingPage>
    <prism:endingPage>14769</prism:endingPage>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/shung/article/2785897">
    <title>Ebola virus matrix protein VP40 uses the COPII transport system for its intracellular transport.</title>
    <link>http://www.citeulike.org/user/shung/article/2785897</link>
    <description>&lt;i&gt;Cell host &#38; microbe, Vol. 3, No. 3. (13 March 2008), pp. 168-177.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The Ebola virus matrix protein VP40 plays an important role in virion formation and viral egress from cells. However, the host cell proteins and mechanisms responsible for intracellular transport of VP40 prior to its contribution to virion formation remain to be elucidated. Therefore we used coimmunoprecipitation and mass spectrometric analyses to identify host proteins interacting with VP40. We found that Sec24C, a component of the host COPII vesicular transport system, interacts specifically with VP40 via VP40 amino acids 303 to 307. Coimmunoprecipitation and dominant-negative mutant studies indicated that the COPII transport system plays a critical role in VP40 intracellular transport to the plasma membrane. Marburg virus VP40 was also shown to use the COPII transport system for intracellular transport. These findings identify a conserved intersection between a host pathway and filovirus replication, an intersection that can be targeted in the development of new antiviral drugs.</description>
    <dc:title>Ebola virus matrix protein VP40 uses the COPII transport system for its intracellular transport.</dc:title>

    <dc:creator>S Yamayoshi</dc:creator>
    <dc:creator>T Noda</dc:creator>
    <dc:creator>H Ebihara</dc:creator>
    <dc:creator>H Goto</dc:creator>
    <dc:creator>Y Morikawa</dc:creator>
    <dc:creator>IS Lukashevich</dc:creator>
    <dc:creator>G Neumann</dc:creator>
    <dc:creator>H Feldmann</dc:creator>
    <dc:creator>Y Kawaoka</dc:creator>
    <dc:identifier>doi:10.1016/j.chom.2008.02.001</dc:identifier>
    <dc:source>Cell host &#38; microbe, Vol. 3, No. 3. (13 March 2008), pp. 168-177.</dc:source>
    <dc:date>2008-05-11T22:21:21-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Cell host &#38; microbe</prism:publicationName>
    <prism:issn>1934-6069</prism:issn>
    <prism:volume>3</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>168</prism:startingPage>
    <prism:endingPage>177</prism:endingPage>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/eddymier/article/2782279">
    <title>Content-Based Music Information Retrieval: Current Directions and Future Challenges</title>
    <link>http://www.citeulike.org/user/eddymier/article/2782279</link>
    <description>&lt;i&gt;Proceedings of the IEEE, Vol. 96, No. 4. (2008), pp. 668-696.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;&#60;para&#62; The steep rise in music downloading over CD sales has created a major shift in the music industry away from physical media formats and towards online products and services. Music is one of the most popular types of online information and there are now hundreds of music streaming and download services operating on the World-Wide Web. Some of the music collections available are approaching the scale of ten million tracks and this has posed a major challenge for searching, retrieving, and organizing music content. Research efforts in music information retrieval have involved experts from music perception, cognition, musicology, engineering, and computer science engaged in truly interdisciplinary activity that has resulted in many proposed algorithmic and methodological solutions to music search using content-based methods. This paper outlines the problems of content-based music information retrieval and explores the state-of-the-art methods using audio cues (e.g., query by humming, audio fingerprinting, content-based music retrieval) and other cues (e.g., music notation and symbolic representation), and identifies some of the major challenges for the coming years. &#60;/para&#62;</description>
    <dc:title>Content-Based Music Information Retrieval: Current Directions and Future Challenges</dc:title>

    <dc:creator>MA Casey</dc:creator>
    <dc:creator>R Veltkamp</dc:creator>
    <dc:creator>M Goto</dc:creator>
    <dc:creator>M Leman</dc:creator>
    <dc:creator>C Rhodes</dc:creator>
    <dc:creator>M Slaney</dc:creator>
    <dc:identifier>doi:10.1109/JPROC.2008.916370</dc:identifier>
    <dc:source>Proceedings of the IEEE, Vol. 96, No. 4. (2008), pp. 668-696.</dc:source>
    <dc:date>2008-05-10T02:46:50-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Proceedings of the IEEE</prism:publicationName>
    <prism:volume>96</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>668</prism:startingPage>
    <prism:endingPage>696</prism:endingPage>
    <prism:category>information</prism:category>
    <prism:category>music</prism:category>
    <prism:category>retrieval</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/Kyaita/article/2753650">
    <title>A retrospective review of 226 hospitalized patients with fever.</title>
    <link>http://www.citeulike.org/user/Kyaita/article/2753650</link>
    <description>&lt;i&gt;Internal medicine (Tokyo, Japan), Vol. 46, No. 1. (2007), pp. 17-22.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;OBJECTIVE: To describe characteristics and outcomes for patients hospitalized with fever, not only patients with fever of unknown origin (FUO). METHODS: Medical records were reviewed for 226 consecutive patients hospitalized in a Japanese referral hospital with fever as one of the clinical problems. RESULTS: Although the majority of illnesses involved some sort of infection (54%), noninfectious inflammatory diseases, particularly adult Still's disease (n=6) and primary vasculitis syndromes (n=5) including 3 cases of Behçet's disease, represented the leading cause in patients who met the definition of FUO [16/51(31%)]. Tuberculosis (n=6) and psychological disorders (n=6) were associated with late diagnosis. However, there was only one patient meeting the definition of FUO among those with a psychological disorder. Among the patients with prolonged fever who did not strictly meet the definition of FUO, there was a considerable number of patients with critical illnesses, such as intra-abdominal abscess, polymyalgia rheumatica, sarcoidosis, ulcerative colitis, Castleman's disease, hematological and solid malignancies, and panhypopituitarism. Drug-induced fever, systemic viral infection and unspecified vasculitis were difficult to definitively diagnose, although these pathologies were suspected as causes of fever. Follow-up of patients without definitive diagnosis at discharge confirmed that the fever subsided spontaneously or the cause of fever was properly treated after diagnosis in every patient and that none died of the underlying febrile illness. CONCLUSIONS: The present findings, from all patients displaying fever at hospitalization, are in agreement with findings from prior FUO series. Strict use of the definition of FUO is thus unwarranted when managing patients with prolonged fever.</description>
    <dc:title>A retrospective review of 226 hospitalized patients with fever.</dc:title>

    <dc:creator>M Goto</dc:creator>
    <dc:creator>H Koyama</dc:creator>
    <dc:creator>O Takahashi</dc:creator>
    <dc:creator>T Fukui</dc:creator>
    <dc:source>Internal medicine (Tokyo, Japan), Vol. 46, No. 1. (2007), pp. 17-22.</dc:source>
    <dc:date>2008-05-04T15:26:20-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Internal medicine (Tokyo, Japan)</prism:publicationName>
    <prism:issn>1349-7235</prism:issn>
    <prism:volume>46</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>17</prism:startingPage>
    <prism:endingPage>22</prism:endingPage>
    <prism:category>fuo</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/MllePapillon/article/2724577">
    <title>Tetraspanins CD9 and CD81 function to prevent the fusion of mononuclear phagocytes</title>
    <link>http://www.citeulike.org/user/MllePapillon/article/2724577</link>
    <description>&lt;i&gt;J. Cell Biol., Vol. 161, No. 5. (9 June 2003), pp. 945-956.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Tetraspanins CD9 and CD81 facilitate the fusion between gametes, myoblasts, or virus-infected cells. Here, we investigated the role of these tetraspanins in the fusion of mononuclear phagocytes. Expression of CD9 and CD81 and their complex formation with integrins were up-regulated when blood monocytes were cultured under normal conditions. Under fusogenic conditions in the presence of Con A, CD9 and CD81 up-regulation was inhibited, and their complex formation with integrins was down-regulated. Anti-CD9 and -CD81 antibodies, which were previously shown to inhibit the fusion of gametes, myoblasts, and virus-infected cells, unexpectedly promoted the fusion of monocytes and alveolar macrophages. However, these effects were not due to altered cell adhesion, aggregation, or cytokine production. When stimulated in vitro or in vivo, alveolar macrophages and bone marrow cells of CD9- and CD81-null mice formed larger numbers of multinucleated cells than those of wild-type mice. Finally, CD9/CD81 double-null mice spontaneously developed multinucleated giant cells in the lung and showed enhanced osteoclastogenesis in the bone. These results suggest that CD9 and CD81 coordinately prevent the fusion of mononuclear phagocytes. 10.1083/jcb.200212031</description>
    <dc:title>Tetraspanins CD9 and CD81 function to prevent the fusion of mononuclear phagocytes</dc:title>

    <dc:creator>Yoshito Takeda</dc:creator>
    <dc:creator>Isao Tachibana</dc:creator>
    <dc:creator>Kenji Miyado</dc:creator>
    <dc:creator>Masatoshi Kobayashi</dc:creator>
    <dc:creator>Toru Miyazaki</dc:creator>
    <dc:creator>Toshiki Funakoshi</dc:creator>
    <dc:creator>Hiromi Kimura</dc:creator>
    <dc:creator>Hiroyuki Yamane</dc:creator>
    <dc:creator>Yoshiyuki Saito</dc:creator>
    <dc:creator>Hiroyuki Goto</dc:creator>
    <dc:creator>Tsutomu Yoneda</dc:creator>
    <dc:creator>Mitsuhiro Yoshida</dc:creator>
    <dc:creator>Toru Kumagai</dc:creator>
    <dc:creator>Tadashi Osaki</dc:creator>
    <dc:creator>Seiji Hayashi</dc:creator>
    <dc:creator>Ichiro Kawase</dc:creator>
    <dc:creator>Eisuke Mekada</dc:creator>
    <dc:identifier>doi:10.1083/jcb.200212031</dc:identifier>
    <dc:source>J. Cell Biol., Vol. 161, No. 5. (9 June 2003), pp. 945-956.</dc:source>
    <dc:date>2008-04-27T19:36:55-00:00</dc:date>
    <prism:publicationYear>2003</prism:publicationYear>
    <prism:publicationName>J. Cell Biol.</prism:publicationName>
    <prism:volume>161</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>945</prism:startingPage>
    <prism:endingPage>956</prism:endingPage>
    <prism:category>cd9</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/loewentigger/article/2699488">
    <title>Nonlinear optimal control applied to STATCOM for power system stabilization</title>
    <link>http://www.citeulike.org/user/loewentigger/article/2699488</link>
    <description>&lt;i&gt;Transmission and Distribution Conference and Exhibition 2002: Asia Pacific. IEEE/PES, Vol. 1 (2002), pp. 342-347 vol.1.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;This paper presents the results of simulator test for improvement of power system stability by applying a nonlinear optimal control to a static synchronous compensator (STATCOM). The STATCOM using the self-commutated converter was selected for this study among FACTS devices, and the power system oscillation damping control and voltage control were designed by using the approach of nonlinear optimal control based on the differential geometry theory. The capability of STATCOM supplies the reactive power at low voltage is larger than conventional SVC, and reactive power of STATCOM can be controlled continuously at high speed. The stabilizing control system was investigated supposing that STATCOM is used in the nonlinear operating points. Specifically, the stabilizing effects by nonlinear control theory were compared with the effects by linear control theory. It was confirmed that nonlinear control was more effective compared with linear control. Moreover, system conditions where nonlinear control operates effectively were clarified.</description>
    <dc:title>Nonlinear optimal control applied to STATCOM for power system stabilization</dc:title>

    <dc:creator>M Sekoguchi</dc:creator>
    <dc:creator>H Konishi</dc:creator>
    <dc:creator>M Goto</dc:creator>
    <dc:creator>A Yokoyama</dc:creator>
    <dc:creator>Q Lu</dc:creator>
    <dc:identifier>doi:10.1109/TDC.2002.1178356</dc:identifier>
    <dc:source>Transmission and Distribution Conference and Exhibition 2002: Asia Pacific. IEEE/PES, Vol. 1 (2002), pp. 342-347 vol.1.</dc:source>
    <dc:date>2008-04-22T08:18:23-00:00</dc:date>
    <prism:publicationYear>2002</prism:publicationYear>
    <prism:publicationName>Transmission and Distribution Conference and Exhibition 2002: Asia Pacific. IEEE/PES</prism:publicationName>
    <prism:volume>1</prism:volume>
    <prism:startingPage>342</prism:startingPage>
    <prism:endingPage>347 vol.1</prism:endingPage>
    <prism:category>energiesystem</prism:category>
    <prism:category>regelung</prism:category>
    <prism:category>stabilitaet</prism:category>
    <prism:category>statcom</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jyuh/article/2691412">
    <title>Role of diacylglycerol kinase in cellular regulatory processes: a new regulator for cardiomyocyte hypertrophy.</title>
    <link>http://www.citeulike.org/user/jyuh/article/2691412</link>
    <description>&lt;i&gt;Pharmacology &#38; therapeutics, Vol. 115, No. 3. (September 2007), pp. 352-359.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Diacylglycerol (DAG) kinase (DGK) phosphorylates and converts DAG to phosphatidic acid. DGK regulates cellular DAG levels and attenuates DAG signaling. The 10 mammalian DGK isoforms have been identified to date. In cardiac myocytes, DGKalpha, epsilon, and zeta are expressed, and DGKzeta is the predominant isoform. DGKzeta inhibits protein kinase C (PKC) activation and subsequent hypertrophic programs in response to endothelin-1 (ET-1) in neonatal rat cardiomyocytes. DGKzeta blocks cardiac hypertrophy induced by G protein-coupled receptor agonists and pressure overload in vivo. DGKzeta attenuates ventricular remodeling and improves survival after myocardial infarction. These data provide a novel insight for subcellular mechanisms of cardiac hypertrophy and heart failure, and DGKzeta may be a new therapeutic target to prevent cardiac hypertrophy and progression to heart failure.</description>
    <dc:title>Role of diacylglycerol kinase in cellular regulatory processes: a new regulator for cardiomyocyte hypertrophy.</dc:title>

    <dc:creator>Y Takeishi</dc:creator>
    <dc:creator>K Goto</dc:creator>
    <dc:creator>I Kubota</dc:creator>
    <dc:identifier>doi:10.1016/j.pharmthera.2007.04.010</dc:identifier>
    <dc:source>Pharmacology &#38; therapeutics, Vol. 115, No. 3. (September 2007), pp. 352-359.</dc:source>
    <dc:date>2008-04-20T00:07:23-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Pharmacology &#38; therapeutics</prism:publicationName>
    <prism:issn>0163-7258</prism:issn>
    <prism:volume>115</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>352</prism:startingPage>
    <prism:endingPage>359</prism:endingPage>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/dietlein/article/2682607">
    <title>Single-layer dipole array for linear-to-circular polarisation conversion of slotted waveguide array</title>
    <link>http://www.citeulike.org/user/dietlein/article/2682607</link>
    <description>&lt;i&gt;IEE Proceedings on Microwaves, Antennas and Propagation, Vol. 143, No. 3. (1996), pp. 211-216.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;A single-layer linear-to-circular polarisation converter is proposed for an application to a slotted waveguide planar array. It consists of dipoles which closely couple to slot arrays. The method of moments clarifies the mutual coupling between the dipoles and the slots on the waveguide. Numerical results promise the use of a uniform and parallel dipole array as a single-layer linear-to-circular polarisation converter for an existing linearly polarised slotted waveguide array. The measurements using a linearly polarised slotted waveguide array in 22.0 GHz band confirm the prediction; the axial ratio less than 1 dB and a negligible insertion loss is realised</description>
    <dc:title>Single-layer dipole array for linear-to-circular polarisation conversion of slotted waveguide array</dc:title>

    <dc:creator>KS Min</dc:creator>
    <dc:creator>J Hirokawa</dc:creator>
    <dc:creator>K Sakurai</dc:creator>
    <dc:creator>M Ando</dc:creator>
    <dc:creator>N Goto</dc:creator>
    <dc:source>IEE Proceedings on Microwaves, Antennas and Propagation, Vol. 143, No. 3. (1996), pp. 211-216.</dc:source>
    <dc:date>2008-04-17T15:50:55-00:00</dc:date>
    <prism:publicationYear>1996</prism:publicationYear>
    <prism:publicationName>IEE Proceedings on Microwaves, Antennas and Propagation</prism:publicationName>
    <prism:volume>143</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>211</prism:startingPage>
    <prism:endingPage>216</prism:endingPage>
    <prism:category>polarizer</prism:category>
    <prism:category>thesisref</prism:category>
    <prism:category>waveguide</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/helsley/article/2679418">
    <title>Bayesian network and nonparametric heteroscedastic regression for nonlinear modeling of genetic network</title>
    <link>http://www.citeulike.org/user/helsley/article/2679418</link>
    <description>&lt;i&gt;Bioinformatics Conference, 2002. Proceedings. IEEE Computer Society (2002), pp. 219-227.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;We propose a new statistical method for constructing a genetic network from microarray gene expression data by using a Bayesian network. An essential point of Bayesian network construction is in the estimation of the conditional distribution of each random variable. We consider fitting nonparametric regression models with heterogeneous error variances to the microarray gene expression data to capture the nonlinear structures between genes. A problem still remains to be solved in selecting an optimal graph, which gives the best representation of the system among genes. We theoretically derive a new graph selection criterion from Bayes approach in general situations. The proposed method includes previous methods based on Bayesian networks. We demonstrate the effectiveness of the proposed method through the analysis of Saccharomyces cerevisiae gene expression data newly obtained by disrupting 100 genes.</description>
    <dc:title>Bayesian network and nonparametric heteroscedastic regression for nonlinear modeling of genetic network</dc:title>

    <dc:creator>S Imoto</dc:creator>
    <dc:creator>Kim Sunyong</dc:creator>
    <dc:creator>T Goto</dc:creator>
    <dc:creator>S Aburatani</dc:creator>
    <dc:creator>K Tashiro</dc:creator>
    <dc:creator>S Kuhara</dc:creator>
    <dc:creator>S Miyano</dc:creator>
    <dc:identifier>doi:10.1109/CSB.2002.1039344</dc:identifier>
    <dc:source>Bioinformatics Conference, 2002. Proceedings. IEEE Computer Society (2002), pp. 219-227.</dc:source>
    <dc:date>2008-04-17T02:28:24-00:00</dc:date>
    <prism:publicationYear>2002</prism:publicationYear>
    <prism:publicationName>Bioinformatics Conference, 2002. Proceedings. IEEE Computer Society</prism:publicationName>
    <prism:startingPage>219</prism:startingPage>
    <prism:endingPage>227</prism:endingPage>
    <prism:category>no-tag</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/asterix77/article/2679047">
    <title>A predominant-F&#60;sub&#62;0&#60;/sub&#62; estimation method for CD recordings: MAP estimation using EM algorithm for adaptive tone models</title>
    <link>http://www.citeulike.org/user/asterix77/article/2679047</link>
    <description>&lt;i&gt;Acoustics, Speech, and Signal Processing, 2001. Proceedings. (ICASSP '01). 2001 IEEE International Conference on, Vol. 5 (2001), pp. 3365-3368 vol.5.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;This paper describes a predominant-F&#60;sub&#62;0&#60;/sub&#62; (fundamental frequency) estimation method called PreFEst, which can detect melody and bass lines in monaural audio signals containing sounds of various instruments, While most previous methods premised mixtures of a few sounds and had difficulty dealing with such complex signals, our method can estimate the F&#60;sub&#62;0&#60;/sub&#62; of the melody and bass lines without assuming the number of sound sources in compact-disc recordings. In this paper we propose the following three extensions to our previous PreFEst to make it more adaptive and flexible: introducing multiple harmonic-structure tone models, estimating the shape of tone models, and introducing a prior distribution of its shape and F&#60;sub&#62;0&#60;/sub&#62; estimates These extensions were implemented by the MAP (maximum a posteriori probability) estimation by using the expectation-maximization algorithm. Experimental results with compact-disc recordings showed that our real-time system based on the extended PreFEst achieved performance improvement</description>
    <dc:title>A predominant-F&#60;sub&#62;0&#60;/sub&#62; estimation method for CD recordings: MAP estimation using EM algorithm for adaptive tone models</dc:title>

    <dc:creator>M Goto</dc:creator>
    <dc:identifier>doi:10.1109/ICASSP.2001.940380</dc:identifier>
    <dc:source>Acoustics, Speech, and Signal Processing, 2001. Proceedings. (ICASSP '01). 2001 IEEE International Conference on, Vol. 5 (2001), pp. 3365-3368 vol.5.</dc:source>
    <dc:date>2008-04-16T21:53:25-00:00</dc:date>
    <prism:publicationYear>2001</prism:publicationYear>
    <prism:publicationName>Acoustics, Speech, and Signal Processing, 2001. Proceedings. (ICASSP '01). 2001 IEEE International Conference on</prism:publicationName>
    <prism:volume>5</prism:volume>
    <prism:startingPage>3365</prism:startingPage>
    <prism:endingPage>3368 vol.5</prism:endingPage>
    <prism:category>6820</prism:category>
    <prism:category>transcription</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/dchughes/article/2673802">
    <title>Phylogenetic relationships among cetaceans revealed by Y-chromosome sequences.</title>
    <link>http://www.citeulike.org/user/dchughes/article/2673802</link>
    <description>&lt;i&gt;Zoological science, Vol. 24, No. 7. (July 2007), pp. 723-732.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The Y chromosome has recently come into the spotlight as a new and efficient genetic marker for tracing paternal lineages. We reconstructed cetacean phylogeny using a 1.7-kbp fragment of the non-recombining Y chromosome (NRY), including the SRY gene and a flanking non-coding region. The topology of the Y-chromosome tree is robust to various methods of analysis and exhibits high branch-support values, possibly due to the absence of recombination, small effective population size, and low homoplasy. The Y-chromosome tree indicates monophyly of each suborder, Mysticeti and Odontoceti, with high branch support values (BS&#62; or =86%; PP&#62; or =98%). In the Odontoceti clade, three superfamilies, Physeteroidea, Ziphioidea, and Delphinoidea, diverged soon after the split between Mysticeti and Odontoceti. Our analysis allows resolution of this rapid radiation and indicates that Physeteroidea is basal in the Odontoceti clade (BS, 99%; PP, 100%; MBS, 61%). The major split within the superfamily Delphinoidea is between the Delphinidae clade and the Monodontidae+ Phocoenidae clade. The phylogenetic relationships among delphinid species are ambiguous, probably because of the rapid radiation of this family. In the Mysticeti clade, the first major split is between Balaenidae and Balaenopteridae; within Balaenopteridae, a Balaenoptera acutorostrata+B. bonaerensis (minke whales) clade forms a sister clade with the other balaenopterid species. Megaptera novaeangliae is nested within Balaenoptera, making the latter paraphyletic. The low homoplasy exhibited by the Y-chromosome data presented here suggests that an extended data set incorporating longer sequences would provide better resolution of cetacean lower-level pylogeny.</description>
    <dc:title>Phylogenetic relationships among cetaceans revealed by Y-chromosome sequences.</dc:title>

    <dc:creator>S Nishida</dc:creator>
    <dc:creator>M Goto</dc:creator>
    <dc:creator>LA Pastene</dc:creator>
    <dc:creator>N Kanda</dc:creator>
    <dc:creator>H Koike</dc:creator>
    <dc:identifier>doi:10.2108/zsj.24.723</dc:identifier>
    <dc:source>Zoological science, Vol. 24, No. 7. (July 2007), pp. 723-732.</dc:source>
    <dc:date>2008-04-15T15:43:20-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Zoological science</prism:publicationName>
    <prism:issn>0289-0003</prism:issn>
    <prism:volume>24</prism:volume>
    <prism:number>7</prism:number>
    <prism:startingPage>723</prism:startingPage>
    <prism:endingPage>732</prism:endingPage>
    <prism:category>cetaceans</prism:category>
    <prism:category>molecular-phylogenetics</prism:category>
    <prism:category>y-chromosome</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/operon/article/2662434">
    <title>Causal analysis of CpG suppression in the Mycoplasma genome.</title>
    <link>http://www.citeulike.org/user/operon/article/2662434</link>
    <description>&lt;i&gt;Microbial &#38; comparative genomics, Vol. 5, No. 1. (2000), pp. 51-58.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Some bacterial genomes are known to have low CpG dinucleotide frequencies. While their causes are not clearly understood, the frequency of CpG is suppressed significantly in the genome of Mycoplasma genitalium, but not in that of Mycoplasma pneumoniae. We compared orthologous gene pairs of the two closely related species to analyze CpG substitution patterns between these two genomes. We also divided genome sequences into three regions: protein-coding, noncoding, and RNA-coding, and obtained the CpG frequencies for each region for each organism. It was found that the observed/expected ratio of CpG dinucleotides is low in both the protein-coding and noncoding regions; while that ratio is in the normal range in the RNA-coding region. Our results indicate that CpG suppression of the Mycoplasma genome is not caused by (1) biased usage amino acid; (2) biased usage of synonymous codon; or (3) methylation effects by the CpG methyltransferase in the genomes of their hosts. Instead, we consider it likely that a certain global pressure, such as genome-wide pressure for the advantages of DNA stability or replication, has the effect of decreasing CpG over the entire genome, which, in turn, resulted in the biased codon usage.</description>
    <dc:title>Causal analysis of CpG suppression in the Mycoplasma genome.</dc:title>

    <dc:creator>M Goto</dc:creator>
    <dc:creator>T Washio</dc:creator>
    <dc:creator>M Tomita</dc:creator>
    <dc:identifier>doi:10.1089/10906590050145267</dc:identifier>
    <dc:source>Microbial &#38; comparative genomics, Vol. 5, No. 1. (2000), pp. 51-58.</dc:source>
    <dc:date>2008-04-12T22:55:40-00:00</dc:date>
    <prism:publicationYear>2000</prism:publicationYear>
    <prism:publicationName>Microbial &#38; comparative genomics</prism:publicationName>
    <prism:issn>1090-6592</prism:issn>
    <prism:volume>5</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>51</prism:startingPage>
    <prism:endingPage>58</prism:endingPage>
    <prism:category>genometrics</prism:category>
    <prism:category>master</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/ceegrs2/article/2650384">
    <title>A 1.5-W single-chip MPEG-2 MP@ML video encoder with low power motion estimation and clocking</title>
    <link>http://www.citeulike.org/user/ceegrs2/article/2650384</link>
    <description>&lt;i&gt;Solid-State Circuits, IEEE Journal of, Vol. 32, No. 11. (1997), pp. 1807-1816.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;A 1.5-W single-chip MPEG-2 MP@ML real-time video encoder large scale integrated circuit (LSI) has been developed. To form an MPEG-2 encoder system, we employ two 16-Mb synchronous DRAM's, a microprocessor unit (MPU), and an audio encoder LSI. Owing to a two-step hierarchical search scheme and a novel adaptive search window scheme, the search range of motion estimation is -48/+47 horizontal and -96/+15.5 vertical, and the pseudo search range, which is the size when the location of the search window is adaptively shifted, is -96/+95 horizontal and -32/+31.5 vertical. We have also developed low-power clocking techniques, i.e., demand-clock controller, local-clock controller, and low-power flip-flops, which can eliminate waste of power in clocking. We have successfully fabricated these new designs as a low-power single-chip MPEG-2 encoder LSI. The operating frequency except for a synchronous DRAM interface unit and a video in/out unit is 54 MHz. The supply voltage to the first and second search engines in a motion estimation unit can be successfully lowered to 2.5 V and the others are 3.3 V. Into a 12.45&#215;12.45 mm&#60;sup&#62;2&#60;/sup&#62; chip with 0.35-&#956;m CMOS and triple-metal layer technology are integrated 3.1 M transistors</description>
    <dc:title>A 1.5-W single-chip MPEG-2 MP@ML video encoder with low power motion estimation and clocking</dc:title>

    <dc:creator>M Mizuno</dc:creator>
    <dc:creator>Y Ooi</dc:creator>
    <dc:creator>N Hayashi</dc:creator>
    <dc:creator>J Goto</dc:creator>
    <dc:creator>M Hozumi</dc:creator>
    <dc:creator>K Furuta</dc:creator>
    <dc:creator>A Shibayama</dc:creator>
    <dc:creator>Y Nakazawa</dc:creator>
    <dc:creator>O Ohnishi</dc:creator>
    <dc:creator>O Ohnishi</dc:creator>
    <dc:creator>Shu-Yu Zhu</dc:creator>
    <dc:creator>A10</dc:creator>
    <dc:creator>Y Yokoyama</dc:creator>
    <dc:creator>A11</dc:creator>
    <dc:creator>Y Katayama</dc:creator>
    <dc:creator>A12</dc:creator>
    <dc:creator>H Takano</dc:creator>
    <dc:creator>A13</dc:creator>
    <dc:creator>N Miki</dc:creator>
    <dc:creator>A14</dc:creator>
    <dc:creator>Y Senda</dc:creator>
    <dc:creator>A15</dc:creator>
    <dc:creator>I Tamitani</dc:creator>
    <dc:creator>A16</dc:creator>
    <dc:creator>M Yamashina</dc:creator>
    <dc:creator>A17</dc:creator>
    <dc:identifier>doi:10.1109/4.641704</dc:identifier>
    <dc:source>Solid-State Circuits, IEEE Journal of, Vol. 32, No. 11. (1997), pp. 1807-1816.</dc:source>
    <dc:date>2008-04-10T19:25:06-00:00</dc:date>
    <prism:publicationYear>1997</prism:publicationYear>
    <prism:publicationName>Solid-State Circuits, IEEE Journal of</prism:publicationName>
    <prism:volume>32</prism:volume>
    <prism:number>11</prism:number>
    <prism:startingPage>1807</prism:startingPage>
    <prism:endingPage>1816</prism:endingPage>
    <prism:category>architecture</prism:category>
    <prism:category>motion-estimation</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/irenas/article/332264">
    <title>The KEGG resource for deciphering the genome.</title>
    <link>http://www.citeulike.org/user/irenas/article/332264</link>
    <description>&lt;i&gt;Nucleic Acids Res, Vol. 32, No. Database issue. (1 January 2004)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;A grand challenge in the post-genomic era is a complete computer representation of the cell and the organism, which will enable computational prediction of higher-level complexity of cellular processes and organism behavior from genomic information. Toward this end we have been developing a knowledge-based approach for network prediction, which is to predict, given a complete set of genes in the genome, the protein interaction networks that are responsible for various cellular processes. KEGG at http://www.genome.ad.jp/kegg/ is the reference knowledge base that integrates current knowledge on molecular interaction networks such as pathways and complexes (PATHWAY database), information about genes and proteins generated by genome projects (GENES/SSDB/KO databases) and information about biochemical compounds and reactions (COMPOUND/GLYCAN/REACTION databases). These three types of database actually represent three graph objects, called the protein network, the gene universe and the chemical universe. New efforts are being made to abstract knowledge, both computationally and manually, about ortholog clusters in the KO (KEGG Orthology) database, and to collect and analyze carbohydrate structures in the GLYCAN database.</description>
    <dc:title>The KEGG resource for deciphering the genome.</dc:title>

    <dc:creator>M Kanehisa</dc:creator>
    <dc:creator>S Goto</dc:creator>
    <dc:creator>S Kawashima</dc:creator>
    <dc:creator>Y Okuno</dc:creator>
    <dc:creator>M Hattori</dc:creator>
    <dc:source>Nucleic Acids Res, Vol. 32, No. Database issue. (1 January 2004)</dc:source>
    <dc:date>2005-09-26T01:48:28-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>Nucleic Acids Res</prism:publicationName>
    <prism:issn>1362-4962</prism:issn>
    <prism:volume>32</prism:volume>
    <prism:number>Database issue</prism:number>
    <prism:category>db</prism:category>
    <prism:category>new</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/nelmor/article/2615392">
    <title>Dopamine-dependent interactions between limbic and prefrontal cortical plasticity in the nucleus accumbens: disruption by cocaine sensitization.</title>
    <link>http://www.citeulike.org/user/nelmor/article/2615392</link>
    <description>&lt;i&gt;Neuron, Vol. 47, No. 2. (21 July 2005), pp. 255-266.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The prefrontal cortex and the hippocampus exhibit converging projections to the nucleus accumbens and have functional reciprocal connections via indirect pathways. As a result, information processing between these structures is likely to be bidirectional. Using evoked potential measures, we examined the interactions of these inputs on synaptic plasticity within the accumbens. Our results show that the direction of information flow between the prefrontal cortex and limbic structures determines the synaptic plasticity that these inputs exhibit within the accumbens. Moreover, this synaptic plasticity at hippocampal and prefrontal inputs selectively involves dopamine D1 and D2 activation or inactivation, respectively. Repeated cocaine administration disrupted this synaptic plasticity at hippocampal and prefrontal cortical inputs and goal-directed behavior in the spatial maze task. Thus, interactions of limbic-prefrontal cortical synaptic plasticity and its dysfunction within the accumbens could underlie complex information processing deficits observed in individuals following psychostimulant administration.</description>
    <dc:title>Dopamine-dependent interactions between limbic and prefrontal cortical plasticity in the nucleus accumbens: disruption by cocaine sensitization.</dc:title>

    <dc:creator>Y Goto</dc:creator>
    <dc:creator>AA Grace</dc:creator>
    <dc:identifier>doi:10.1016/j.neuron.2005.06.017</dc:identifier>
    <dc:source>Neuron, Vol. 47, No. 2. (21 July 2005), pp. 255-266.</dc:source>
    <dc:date>2008-03-31T08:33:26-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Neuron</prism:publicationName>
    <prism:issn>0896-6273</prism:issn>
    <prism:volume>47</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>255</prism:startingPage>
    <prism:endingPage>266</prism:endingPage>
    <prism:category>cocaine</prism:category>
    <prism:category>dopamine</prism:category>
    <prism:category>drugs</prism:category>
    <prism:category>hippocampus</prism:category>
    <prism:category>pfc</prism:category>
    <prism:category>plasticity</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/nelmor/article/210656">
    <title>Dopaminergic modulation of limbic and cortical drive of nucleus accumbens in goal-directed behavior</title>
    <link>http://www.citeulike.org/user/nelmor/article/210656</link>
    <description>&lt;i&gt;Nature Neuroscience, Vol. 8, No. 6. (22 May 2005), pp. 805-812.&lt;/i&gt;</description>
    <dc:title>Dopaminergic modulation of limbic and cortical drive of nucleus accumbens in goal-directed behavior</dc:title>

    <dc:creator>Yukiori Goto</dc:creator>
    <dc:creator>Anthony Grace</dc:creator>
    <dc:identifier>doi:10.1038/nn1471</dc:identifier>
    <dc:source>Nature Neuroscience, Vol. 8, No. 6. (22 May 2005), pp. 805-812.</dc:source>
    <dc:date>2005-05-25T19:50:13-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Nature Neuroscience</prism:publicationName>
    <prism:issn>1097-6256</prism:issn>
    <prism:volume>8</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>805</prism:startingPage>
    <prism:endingPage>812</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>dopamine</prism:category>
    <prism:category>hippocampus</prism:category>
    <prism:category>pfc</prism:category>
    <prism:category>ventral_striatum</prism:category>
</item>



</rdf:RDF>

